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TUCoPS :: Wetware Hacking :: Others :: smartdr2.txt

LaTeX format of references to "Smart Drugs"




From news.funet.fi!sunic!mcsun!unido!fauern!ira.uka.de!sol.ctr.columbia.edu!zaphod.mps.ohio-state.ed.hp.com!elroy.jpl.nasa.gov!jarthur!nntp-server.caltech.edu!nntp-server.caltech.edu!bard Sun Apr 11:253 EET DST 1991
Article: 12719 of sci.med
Xref: jyu.fi sci.med:12719 alt.drugs:8871
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From: bard@beyond.cs.caltech.edu (Stephen Philip Bard)
Newsgroups: sci.med,alt.drugs
Subject: LaTeX format of references to "Smart Drugs"
Message-ID: <BARD.91Apr21012422@beyond.cs.caltech.edu>
Date: 21 Apr 91 08:24:22 GMT
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In-Reply-To: twk@cadence.com's message of 17 Apr 91 18:11:43 GMT


              (Quinuclidinyl Benzilate); 70-22-4 (Oxotremorine); 7491-74-9
              (Piracetam)

\item [Subject:]     *Aging -- metabolism.
              Animal.
              Atropine -- pharmacology.
              Cerebral Cortex -- drug effects.
             *Cerebral Cortex -- metabolism.
              Female.
              Male.
              Mice.
              Oxotremorine -- pharmacology.
             *Piracetam -- pharmacology.
             *Pyrrolidinones -- pharmacology.
              Quinuclidinyl Benzilate -- pharmacology.
             *Receptors, Muscarinic -- drug effects.
              Scopolamine -- pharmacology.

\item [Abstract:] Chronic treatment (2 weeks) with piracetam (500 mg/kg, once daily PO)
    elevated m-cholinoceptor density in the frontal cortex of aged (18 months)
    female mice by about 30-40\%, but had no effect on m-cholinoceptor density
    in the frontal cortex of young (4 weeks) mice. The effect of piracetam on
    m-cholinoceptor density as determined by the specific binding of tritiated
    QNB was not affected by concomitant daily treatment with either choline
    (200 mg/kg) or scopolamine (4 mg/kg). It is concluded that the effect of
    piracetam on m-cholinoceptor density could explain the positive effects
    which have been reported for combinations of cholinergic precursor
    treatment with piracetam on memory and other cognitive functions in aged
    experimental animals and patients and could also represent part of the
    possible mechanism of action of piracetam alone.


\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Wilsher CR; Bennett D; Chase CH; Conners CK; DiIanni M; Feagans
              L; Hanvik LJ; Helfgott E; Koplewicz H; Overby P.
\item [Title:]        Piracetam and dyslexia: effects on reading tests.
\item [Language:]     English.

\item [Journal:]      Journal of Clinical Psychopharmacology, 1987 Aug, 7(4):230-7.

\item [CAS;EC No.:]   7491-74-9 (Piracetam)

\item [Subject:]      Child.
              Clinical Trials.
              Double-Blind Method.
             *Dyslexia -- drug therapy.
              Dyslexia -- psychology.
              Female.
              Human.
              Male.
              Piracetam -- adverse effects.
             *Piracetam -- therapeutic use.
             *Pyrrolidinones -- therapeutic use.
              Random Allocation.
             *Reading.
              Support, Non-U.S. Gov't.

\item [Abstract:] Previous research has suggested that dyslexics treated with piracetam
    have shown improvements in reading skills, verbal memory and verbal
    conceptualizing ability, feature analysis, and processing of letter-like
    stimuli. Two hundred twenty-five dyslexic children between the ages of 7
    years 6 months and 12 years 11 months whose reading skills were
    significantly below their intellectual capacity were enrolled in a
    multicenter, 36-week, double-blind, placebo-controlled study. Children of
    below average intelligence, with abnormal findings on audiologic,
    ophthalmologic, neurologic, psychiatric, and physical examinations, who
    were emotionally disturbed or educationally deprived and who had recently
    been treated with psychoactive medication were excluded from the trial.
    Piracetam was well tolerated, with no serious adverse clinical or
    laboratory effects reported. Piracetam-treated children showed significant
    improvements in reading ability (Gray Oral Reading Test) and reading
    comprehension (Gilmore Oral Reading Test). Treatment effects were evident
    after 12 weeks and were sustained for the total period (36 weeks).



\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Zhang SS; Zhu TJ; Zhang DS; Chen XY.
\item [Title:]        [Effects of cerebral GABA level on learning and memory].
\item [Language:]     Chinese.

\item [Journal:]      Chung-Kuo Yao Li Hsueh Pao  acta Pharmacologica Sinica , 1989
             Jan, 10(1):10-2.

\item [CAS;EC No.:]   56-12-2 (GABA); 645-88-5 (Aminooxyacetic Acid)

\item [Subject:]      Aminooxyacetic Acid -- pharmacology.
              Animal.
             *Brain Chemistry -- drug effects.
              English Abstract.
              Female.
              GABA -- analysis.
             *GABA -- pharmacology.
              Injections, Intraventricular.
             *Learning -- drug effects.
              Male.
             *Memory -- drug effects.
              Mice.
              Semicarbazides -- pharmacology.
              Support, Non-U.S. Gov't.

\item [Abstract:] In step-down tests, icv GABA 0.1 micrograms (3 min before training)
    or ip amino-oxyacetic acid 20 mg/kg (1.5 h before training) both
    significantly impaired memory acquisition in mice. But semicarbazide (ip
    110 mg/kg 3.5 h before training), an inhibitor of GABA synthesis, improved
    the anisodine-induced impairments of learning. The effects of GABA was also
    enhanced by aminooxyacetic acid. The results suggest that the increase of
    cerebral GABA contents is unfavourable to learning and memory.




1. 
\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Ammassari-Teule M; D'Amato FR; Sansone M; Oliverio A.
\item [Title:]        Avoidance facilitation in adult mice by prenatal administration
              of the nootropic drug oxiracetam.
\item [Language:]     English.

\item [Journal:]      Pharmacol Res Commun, 1986 Dec, 18(12):1169-76.

\item [CAS;EC No.:]   62613-82-5 (oxiracetam)

\item [Subject:]      Animal.
             *Avoidance Learning -- drug effects.
              Female.
              Male.
              Maternal-Fetal Exchange.
              Mice.
              Motor Activity -- drug effects.
              Pregnancy.
             *Pyrrolidines -- pharmacology.

\item [Abstract:] CD-1 mice prenatally exposed to saline solution or to the nootropic
    drug oxiracetam (50 mg/kg during the whole pregnancy) were tested, when
    adults, for locomotor activity and for shuttle-box avoidance acquisition.
    Prenatal drug exposure produced long-lasting effects, evident in mature
    offspring. At the age of two months, mice prenatally exposed to oxiracetam
    showed a slight but significant reduction in locomotor activity. At the age
    of three months, these animals exhibited higher performances than control
    mice in avoidance acquisition.


\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Ammassari-Teule M; D'Amato FR; Sansone M; Oliverio A.
\item [Address:]      Istituto di Psicobiologia e Psicofarmacologia, CNR, Roma, Italy.
\item [Title:]        Enhancement of radial maze performances in CD1 mice after
             prenatal exposure to oxiracetam: possible role of sustained
              investigative responses developed during ontogeny.
\item [Language:]     English.

\item [Journal:]      Physiology and Behavior, 1988, 42(3):281-5.

\item [CAS;EC No.:]   62613-82-5 (oxiracetam)

\item [Subject:]      Animal.
              Arousal -- drug effects.
             *Discrimination Learning -- drug effects.
              Exploratory Behavior -- drug effects.
              Female.
              Mice.
              Mice, Inbred Strains.
              Motor Skills -- drug effects.
             *Orientation -- drug effects.
              Pregnancy.
             *Prenatal Exposure Delayed Effects.
             *Pyrrolidines -- pharmacology.
              Recall -- drug effects.

\item [Abstract:] A longitudinal study aimed at analyzing the behavioral effects of
    prenatal exposure to the nootropic compound oxiracetam was carried out in
    CD1 mice. Two groups of females were injected either with oxiracetam or
    saline from the beginning of pregnancy until parturition. Examination of
    pups from birth until the first month of age revealed no-influence of the
    treatment on litter size, body weights, sensory motor reflexes and
    motility. When placed in the open field at one month of age, mice born by
    mothers exposed to oxiracetam displayed more self grooming and spent less
    time in freezing than control mice. Prenatally treated mice were then found
    more interactive with their environment since the introduction of a novel
    object in the open field was followed by increased ambulation and higher
    sniffing object and rearing object scores. At three months of age, mice
    from both groups were tested in a radial six-arm maze task. Choice accuracy
    was significantly higher in prenatally treated mice which also tended to
    optimize their exploratory sequences by frequently running the maze in a
    clock-wise fashion. These results suggest that the better learning
    performances observed in the experimental group could be viewed as a
    consequence of an enhanced cognitive development based upon the higher rate
    of interactions with the environment shown by prenatally treated mice
    during ontogeny.



\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Kuribara H; Tadokoro S.
\item [Address:]      Division for Behavior Analysis, Gunma University School of
              Medicine, Maebashi, Japan.
\item [Title:]        Facilitating effect of oxiracetam and piracetam on acquisition of
              discrete two-way shuttle avoidance in normal mice.
\item [Language:]     English.

\item [Journal:]      Japanese Journal of Pharmacology, 1988 Dec, 48(4):494-8.

\item [CAS;EC No.:]   62613-82-5 (oxiracetam); 7491-74-9 (Piracetam)

\item [Subject:]      Animal.
             *Avoidance Learning -- drug effects.
              Mice.
              Mice, Inbred BALB C.
              Mice, Inbred Strains.
             *Piracetam -- pharmacology.
             *Pyrrolidines -- pharmacology.
             *Pyrrolidinones -- pharmacology.

\item [Abstract:] Effects of oxiracetam and piracetam on acquisition of the discrete
    two-way shuttle avoidance response were investigated in normal mice of the
    dd strain. When oxiracetam or piracetam was administered only once
    immediately before the training session, the mice showed a greater number
    of avoidance responses in comparison with the saline-treated control mice,
    with the maximum effect at 30 mg/kg of oxiracetam and 100 mg/kg of
    piracetam. These results suggest that oxiracetam and piracetam facilitate
    the avoidance acquisition in normal mice.




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Maina G; Fiori L; Torta R; Fagiani MB; Ravizza L; Bonavita E;
              Ghiazza B; Teruzzi F; Zagnoni PG; Ferrario E; et al.
\item [Address:]      Clinica Psichiatrica, Universita di Torino, Italia.
\item [Title:]        Oxiracetam in the treatment of primary degenerative and
             multi-infarct dementia: a double-blind, placebo-controlled study.
\item [Language:]     English.

\item [Journal:]      Neuropsychobiology, 1989, 21(3):141-5.

\item [CAS;EC No.:]   62613-82-5 (oxiracetam)

\item [Subject:]      Aged.
              Aged, 80 and over.
             *Dementia, Multi-Infarct -- drug therapy.
             *Dementia, Presenile -- drug therapy.
             *Dementia, Senile -- drug therapy.
              Double-Blind Method.
              Female.
              Human.
              Male.
              Middle Age.
              Multicenter Studies.
              Pyrrolidines -- adverse effects.
             *Pyrrolidines -- therapeutic use.
              Time Factors.

\item [Abstract:] A multicentre, double-blind, between-patient study was carried out to
    evaluate the efficacy and tolerability of oxiracetam (800-mg tablets), in
    comparison with placebo, each given twice daily for 12 weeks to patients
    suffering from primary degenerative, multi-infarct or mixed forms of
    dementia. Efficacy was assessed by the Inventory of Psychic and Somatic
    Complaints in the Elderly (IPSC-E), administered at entry and after 4, 8
    and 12 weeks of treatment, and by the Blessed Dementia Scale and the
    Newcastle Memory, Information and Concentration Scale (NMICS), administered
    at the beginning and at the end of the study. Three hundred and seven
    patients were enrolled, 18 of whom were excluded from the analysis because
    of violation of the protocol. Two hundred and eighty-nine patients were
    analyzed (145 m, 144 f, mean age 73 years) and 272 completed the study; 3
    patients in each treatment group were withdrawn because of poor
    tolerability, 10 because of poor compliance and 1 patient because of the
    occurrence of a cerebral stroke. A significantly (p less than 0.01)
    different effect, in favor of oxiracetam, was observed in the three main
    efficacy criteria (i.e. IPSC-E, Blessed Dementia Scale and NMIC total
    scores), and confirmed by descriptive analyses carried out on some subitems
    of the scales used. Thirty-one patients on oxiracetam and 27 on placebo
    complained of a total of 35 and 32 minor unwanted effects, respectively. No
    clinically or statistically significant changes were observed on routine
    laboratory examinations. 




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Murray CL; Fibiger HC.
\item [Title:]        The effect of pramiracetam (CI-879) on the acquisition of a
              radial arm maze task.
\item [Language:]     English.

\item [Journal:]      Psychopharmacology Berlin, 1986, 89(3):378-81.

\item [CAS;EC No.:]   68497-62-1 (pramiracetam)

\item [Subject:]      Animal.
              Brain -- drug effects.
              Cholinergic Fibers -- drug effects.
             *Learning -- drug effects.
              Male.
             *Memory -- drug effects.
              Memory, Short-Term -- drug effects.
             *Pyrrolidines -- pharmacology.
              Rats.
              Space Perception -- drug effects.
              Support, Non-U.S. Gov't.

\item [Abstract:] The effect of the nootropic drug pramiracetam (CI-879) on acquisition
    of a radial arm maze task was examined in the rat. Two doses of
    pramiracetam (7.5 mg/kg and 15 mg/kg) were administered daily prior to
    testing for 7 weeks in a 16-arm radial maze in which nine arms were baited
    with food. This procedure permitted a distinction between working memory
    (short-term) and reference memory (long-term). Both doses of pramiracetam
    significantly improved performance in the reference memory component of the
    task, but did not significantly affect the working memory component. These
    data indicate that pramiracetam can enhance some aspects of spatial
    learning and memory in the rat.




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Drago F; Valerio C; D'Agata V; Astuto C; Spadaro F; Continella G;
              Scapagnini U.
\item [Address:]      Institute of Pharmacology, University of Catania Medical School,
              Italy.
\item [Title:]        Pyroglutamic acid improves learning and memory capacities in old
              rats.
\item [Language:]     English.

\item [Journal:]      Functional Neurology, 1988 Apr-Jun, 3(2):137-43.

\item [CAS;EC No.:]   98-79-3 (Pyrrolidonecarboxylic Acid)

\item [Subject:]     *Aging -- physiology.
              Animal.
              Avoidance Learning -- drug effects.
             *Avoidance Learning -- physiology.
              Injections, Intraperitoneal.
              Male.
              Memory -- drug effects.
             *Memory -- physiology.
             *Pyrrolidinones -- pharmacology.
             *Pyrrolidonecarboxylic Acid -- pharmacology.
              Rats.
              Rats, Inbred Strains.

\item [Abstract:] The effects of the arginine salt of pyroglutamic acid
    (2-oxo-pyrrolidone carboxylic acid, PCA) on learning and memory capacities
    of old rats were studied in a subchronic treatment schedule (i.p. injection
    of 0.1 and 1 g/kg/day for 15 days). The acquisition and extinction of
    active avoidance behaviour were studied in a pole-jumping test situation.
    The retention of passive avoidance response was examined in a step-through
    passive avoidance task. PCA facilitated the rate of acquisition of
    pole-jumping response, and inhibited the extinction of the response. The
    dose of 1 g/kg was more potent than 0.1 g/kg in this respect. Also in the
    passive avoidance task, the treatment with PCA was followed by an
    improvement of avoidance retention. These results indicate that PCA is a
    behaviourally active compound in that it improves learning and memory
    capacities in old rat.




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Grioli S; Lomeo C; Quattropani MC; Spignoli G; Villardita C.
\item [Address:]      Cattedra di Patologia Neurologica II dell'Universita di Catania,
              Italy.
\item [Title:]        Pyroglutamic acid improves the age associated memory impairment.
\item [Language:]     English.

\item [Journal:]      Fundamental and Clinical Pharmacology, 1990, 4(2):169-73.

\item [CAS;EC No.:]   98-79-3 (Pyrrolidonecarboxylic Acid)

\item [Subject:]      Aged.
              Aged, 80 and over.
              Double-Blind Method.
              Form Perception -- drug effects.
              Human.
             *Memory Disorders -- drug therapy.
              Memory Disorders -- psychology.
              Middle Age.
              Psychomotor Performance -- drug effects.
             *Pyrrolidinones -- therapeutic use.
             *Pyrrolidonecarboxylic Acid -- therapeutic use.
              Randomized Controlled Trials.

\item [Abstract:] Pyroglutamic acid (PCA) was compared with placebo in a randomized,
    double blind trial for assessing its efficacy in treating memory deficits
    in 40 aged subjects. Twenty subjects were treated with PCA and 20 with
    placebo over a period of 60 d. Memory functions were evaluated at baseline
    and after 60 d of treatment by means of a battery made up of 6 memory
    tasks. The results suggest that PCA is effective in improving some verbal
    memory functions in subjects affected by age-related memory decline. 




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Moret C; Briley M.
\item [Title:]        The "forgotten" amino acid pyroglutamate [letter].
\item [Language:]     English.

\item [Journal:]      Trends in Pharmacological Sciences, 1988 Aug, 9(8):278-9.

\item [CAS;EC No.:]   98-79-3 (Pyrrolidonecarboxylic Acid)

\item [Subject:]      Animal.
             *Glutamates -- physiology.
              Human.
             *Pyrrolidinones -- physiology.
              Pyrrolidonecarboxylic Acid -- pharmacology.
             *Pyrrolidonecarboxylic Acid -- physiology.





\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Paoli F; Spignoli G; Pepeu G.
\item [Address:]      Department of Preclinical and Clinical Pharmacology, University
              of Florence, Italy.
\item [Title:]        Oxiracetam and D-pyroglutamic acid antagonize a disruption of
              passive avoidance behaviour induced by the N-methyl-D-aspartate
              receptor antagonist 2-amino-5-phosphonovalerate.
\item [Language:]     English.

\item [Journal:]      Psychopharmacology, 1990, 100(1):130-1.

\item [CAS;EC No.:]   0 (N-methyl-D-aspartate receptor); 62613-82-5 (oxiracetam);
              7004-03-7 (Valine); 76326-31-3 (2-amino-5-phosphopentanoic acid);
              98-79-3 (Pyrrolidonecarboxylic Acid)

\item [Subject:]      Animal.
             *Avoidance Learning -- drug effects.
              Injections, Intraventricular.
              Male.
              Motor Activity -- drug effects.
             *Pyrrolidines -- pharmacology.
             *Pyrrolidinones -- pharmacology.
             *Pyrrolidonecarboxylic Acid -- pharmacology.
              Rats.
              Rats, Inbred Strains.
             *Synaptic Receptors -- drug effects.
             *Valine -- analogs \& derivatives.
              Valine -- antagonists \& inhibitors.
              Valine -- pharmacology.

\item [Abstract:] Intracerebroventricular administration (6 micrograms/2 microliters)
    of D-2-amino-5-phosphonovalerate (AP-5), a specific antagonist of the NMDA
    receptors, prior to training impaired the passive avoidance in a retention
    test in rat. Pretreatment with oxiracetam and D-pyroglutamic acid at doses
    ranging from 50 to 500 mg/kg SC dose-dependently prevented the disruptive
    effect of AP-5. This finding indicates that an interaction with excitatory
    amino acid NMDA type receptors may be important in behavioural effects of
    the two pyrrolidinone derivatives. 




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       DeNoble VJ.
\item [Title:]        Vinpocetine enhances retrieval of a step-through passive
              avoidance response in rats.
\item [Language:]     English.

\item [Journal:]      Pharmacology, Biochemistry and Behavior, 1987 Jan, 26(1):183-6.

\item [CAS;EC No.:]   42971-12-0 (ethyl apovincaminate)

\item [Subject:]      Animal.
             *Avoidance Learning -- drug effects.
              Male.
              Memory -- drug effects.
              Rats.
              Rats, Inbred Strains.
             *Vinca Alkaloids -- pharmacology.

\item [Abstract:] Vinpocetine, vincamine, apovincaminic acid, vinconate, aniracetam,
    Hydergine, and pemoline were evaluated for their ability to enhance
    retrieval of a step-through passive avoidance response in rats. The
    percentage of rats performing the avoidance response was found to decrease
    as a function of the number of days between training and retention testing
    (Day 1, 100\%; Day 2, 65\%; Day 3, 23\%; Days 4 and 5, 0\%). Vinpocetine
    administered 60 minutes prior to testing for retention significantly
    increased the number of rats performing the passive avoidance response.
    Retrieval enhancement was dose-related in an inverted U-shaped function
    with the effective doses at 18 and 30 mg/kg PO. In contrast, apovincaminic
    acid (1-400 mg/kg PO), vincamine (1-200 mg/kg PO), vinconate (1-200 mg/kg
    PO), aniracetam (1-300 mg/kg PO), Hydergine (0.1-10 mg/kg PO), and pemoline
    (1-30 mg/kg PO) were not effective. These data support the view that
    vinpocetine has cognition-activating abilities as defined in an animal
    model of memory retrieval.




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       DeNoble VJ; Repetti SJ; Gelpke LW; Wood LM; Keim KL.
\item [Title:]        Vinpocetine: nootropic effects on scopolamine-induced and
              hypoxia-induced retrieval deficits of a step-through passive
              avoidance response in rats.
\item [Language:]     English.

\item [Journal:]      Pharmacology, Biochemistry and Behavior, 1986 Apr, 24(4):1123-8.

\item [CAS;EC No.:]   11032-41-0 (Dihydroergotoxine); 1617-90-9 (Vincamine); 42971-12-0
              (ethyl apovincaminate); 51-34-3 (Scopolamine); 72432-10-1
              (aniracetam)

\item [Subject:]      Animal.
              Avoidance Learning.
              Cerebral Anoxia -- complications.
              Dihydroergotoxine -- therapeutic use.
              Male.
              Memory Disorders -- chemically induced.
             *Memory Disorders -- prevention \& control.
              Pyrrolidinones -- therapeutic use.
              Rats.
              Rats, Inbred Strains.
              Reaction Time.
              Scopolamine.
             *Vinca Alkaloids -- therapeutic use.
              Vincamine -- therapeutic use.

\item [Abstract:] Vinpocetine, vincamine, aniracetam, and Hydergine, compounds with
    purported cognition activating activity, were evaluated for their ability
    to prevent scopolamine-induced and hypoxia-induced impairment of passive
    avoidance retention (24 hr) in rats. Vinpocetine (peak effect dose [PED]=
    200 mg/kg PO), aniracetam (PED = 100 mg/kg PO), vincamine (PED = 30 mg/kg
    PO), and Hydergine (PED = 1 mg/kg PO) prevented memory disruption by
    scopolamine. Vinpocetine (PED = 3 mg/kg PO) and aniracetam (PED = 30 mg/kg
    PO) were also effective in preventing disruption of passive avoidance
    retention impaired by 7\% oxygen hypoxia. In contrast, Hydergine (0.05 to 3
    mg/kg PO) and vincamine (0.3 to 100 mg/kg PO) were not effective against
    hypoxia-induced impairment. Hydergine at doses greater than 10 mg/kg PO
    markedly impaired motor function. In both tests the protection was
    dose-related for all test substances in an inverted U-shaped manner.
    Mecamylamine (1, 3, 10 mg/kg SC), (-)-nicotine (0.1 to 0.4 mg/kg SC),
    apovincaminic acid (1-400 mg/kg PO) and pemoline (1-100 mg/kg PO) did not
    protect against memory impairment induced by either procedure. These data
    support the view that vinpocetine, a compound chemically distinct from the
    pyrrolidinones, has a cognitive activating ability as defined in models of
    both scopolamine-induced and hypoxia-induced memory impairment in rats.




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Bonavita E.
\item [Title:]        Study of the efficacy and tolerability of L-acetylcarnitine
              therapy in the senile brain.
\item [Language:]     English.

\item [Journal:]      International Journal of Clinical Pharmacology, Therapy, and
             Toxicology, 1986 Sep, 24(9):511-6.

\item [CAS;EC No.:]   14992-62-2 (Acetylcarnitine); 541-15-1 (Carnitine)

\item [Subject:]      Acetylcarnitine -- adverse effects.
             *Acetylcarnitine -- therapeutic use.
              Aged.
              Aged, 80 and over.
              Anxiety Disorders -- drug therapy.
             *Carnitine -- analogs \& derivatives.
             *Cerebral Arteriosclerosis -- drug therapy.
              Cognition Disorders -- drug therapy.
              Depression -- drug therapy.
              Double-Blind Method.
              Female.
              Human.
              Male.
              Memory Disorders -- drug therapy.
              Random Allocation.

\item [Abstract:] The aim of this study was to evaluate the efficacy and tolerability
    of L-acetylcarnitine therapy in the senile brain. The trial was conducted
    on a double-blind basis, with a total of 40 patients divided into two
    groups of 20, treated for 40 days with L-acetylcarnitine and placebo,
    respectively--the therapeutic regimen being two 500 mg tablets t.i.d.
    Mental parameters of the senile brain were assessed at 0, 20 and 40 days of
    treatment, while basal and final values were recorded for a number of
    laboratory tests. Statistical analysis of results confirmed that
    short-term, intensive L-acetylcarnitine treatment can determine a
    significant improvement of the main mental parameters of the senile brain,
    without incidence of significant side effects.




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Bossoni G; Carpi C.
\item [Title:]        Effect of acetyl-L-carnitine on conditioned reflex learning rate
              and retention in laboratory animals.
\item [Language:]     English.

\item [Journal:]      Drugs under Experimental and Clinical Research, 1986,
             12(11):911-6.

\item [CAS;EC No.:]   14992-62-2 (Acetylcarnitine); 541-15-1 (Carnitine)

\item [Subject:]     *Acetylcarnitine -- pharmacology.
              Animal.
              Avoidance Learning -- drug effects.
             *Carnitine -- analogs \& derivatives.
              Conditioning, Classical -- drug effects.
              Electroshock.
             *Learning -- drug effects.
              Male.
              Mice.
              Rats.
              Retention (Psychology) -- drug effects.

\item [Abstract:] The aim of the study was to evaluate the effects of
    acetyl-L-carnitine on learning and/or memory processes in laboratory
    animals. In the water maze test, acetyl-L-carnitine, given
    intraperitoneally at doses ranging from 0.3 to 100 mg/kg, improved
    performances in both mice and rats. In the latter the drug also proved
    active when administered orally in the 3-100 mg/kg dosage range. In the
    pole climbing test in the rat, acetyl-L-carnitine at doses ranging from
    0.03 to 10 mg/kg i.p. increased the conditioned reflex learning rate. In
    the passive avoidance test in the rat, significant increases in retention
    were observed after treatment with acetyl-L-carnitine at doses ranging from
    1 to 30 mg/kg i.p. In the passive avoidance plus electroconvulsive shock
    test in the mouse, acetyl-L-carnitine antagonized amnesia at doses ranging
    from 0.1 to 3 mg/kg i.p.




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Passeri M; Cucinotta D; Bonati PA; Iannuccelli M; Parnetti L;
              Senin U.
\item [Address:]      Department of Internal Medicine, University of Parma, Italy.
\item [Title:]        Acetyl-L-carnitine in the treatment of mildly demented elderly
              patients.
\item [Language:]     English.

\item [Journal:]      International Journal of Clinical Pharmacology Research, 1990,
             10(1-2):75-9.

\item [CAS;EC No.:]   14992-62-2 (Acetylcarnitine); 541-15-1 (Carnitine)

\item [Subject:]     *Acetylcarnitine -- therapeutic use.
              Aged.
             *Carnitine -- analogs \& derivatives.
              Cognition -- drug effects.
             *Dementia -- drug therapy.
              Dementia -- psychology.
              Double-Blind Method.
              Female.
              Human.
              Male.
              Randomized Controlled Trials.

\item [Abstract:] It has been hypothesized that acetyl-L-carnitine has a cholinomimetic
    action. It is for this reason that it has been used in the therapy of
    Alzheimer's type senile dementia impairment. In the present controlled
    double-blind study the authors followed two randomized homogeneous groups
    of both sexes of 30 patients each, aged over 65 years and suffering from
    mild mental impairment. One group of patients underwent therapy with
    acetyl-L-carnitine, 2 g/day for three months, while the other group was
    treated with a placebo. The statistical evaluation of the results was
    carried-out using non-parametric methods (Friedman-Nemenyi two-way ANOVA).
    It was possible to affirm that the acetyl-L-carnitine treated patients
    showed statistically significant improvement in the behavioural scales, in
    the memory tests, in the attention barrage test and in the Verbal Fluency
    test. These satisfactory results confirm the therapeutic importance of
    acetyl-L-carnitine in the treatment of elderly patients with mental
    impairment, which could be related principally to acetylcholine defects. 





\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Passeri M; Iannuccelli M; Ciotti G; Bonati PA; Nolfe G; Cucinotta
              D.
\item [Address:]      Department of Internal Medicine, Postgraduate School of
              Gerontology and Geriatrics, University of Parma, Italy.
\item [Title:]        Mental impairment in aging: selection of patients, methods of
              evaluation and therapeutic possibilities of acetyl-L-carnitine.
\item [Language:]     English.

\item [Journal:]      International Journal of Clinical Pharmacology Research, 1988,
             8(5):367-76.

\item [CAS;EC No.:]   14992-62-2 (Acetylcarnitine); 541-15-1 (Carnitine)

\item [Subject:]      Acetylcarnitine -- administration \& dosage.
             *Acetylcarnitine -- therapeutic use.
              Aged.
              Aged, 80 and over.
              Analysis of Variance.
             *Carnitine -- analogs \& derivatives.
              Dementia -- drug therapy.
              Female.
              Human.
              Male.
             *Mental Disorders -- drug therapy.
             *Mental Processes -- drug effects.
              Placebos.

\item [Abstract:] The authors carried out a double-blind study in two randomized
    homogeneous groups of both sexes of 15 patients each, over 65 years of age
    and suffering from mild mental impairment. One group of patients underwent
    therapy with acetyl-L-carnitine, 2 g/day for three months, while the other
    group was treated with a placebo. The statistical evaluation of the results
    were carried out using nonparametric methods (Friedman-Nemenyi two-way
    Anova and Mann Whitney U-Test). However, the two groups did not differ
    significantly in either test at the end of treatment. It is possible to
    affirm that the acetyl-L-carnitine treated patients showed statistically
    significant improvement in the behavioural performances (Blessed Dementia
    Scale p less than 0.02; Stuard Hospital Geriatric Rating Scale p less than
    0.01), in the memory tests (Rey short-term p less than 0.02; Rey long-term
    p less than 0.05; Corsi p less than 0.05), in the attention test (Barrage
    test p less than 0.01) and in the Verbal Fluency test p less than 0.01).




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Drago F; Continella G; Pennisi G; Alloro MC; Calvani M;
              Scapagnini U.
\item [Title:]        Behavioral effects of acetyl-l-carnitine in the male rat.
\item [Language:]     English.

\item [Journal:]      Pharmacology, Biochemistry and Behavior, 1986 May, 24(5):1393-6.

\item [CAS;EC No.:]   14992-62-2 (Acetylcarnitine); 541-15-1 (Carnitine)

\item [Subject:]     *Acetylcarnitine -- pharmacology.
              Animal.
             *Behavior, Animal -- drug effects.
             *Carnitine -- analogs \& derivatives.
              Conditioning, Operant -- drug effects.
              Extinction (Psychology) -- drug effects.
              Injections, Intraperitoneal.
              Injections, Intraventricular.
              Male.
              Memory -- drug effects.
              Motor Activity -- drug effects.
              Rats.
              Rats, Inbred Strains.

\item [Abstract:] The behavioral activity of carnitine acetylate derivative,
    acetyl-l-carnitine has been studied in the male rat. Intraperitoneal (IP)
    injection of acetyl-l-carnitine was followed by an increase in ambulation
    and rearing items in the open field behavior. Both the number of
    conditioned avoidance response (CARs) and the percentage of learners in the
    acquisition of shuttle-box active avoidance behavior appeared to be
    increased by IP or intracerebroventricular (ICV) injection of the drug at
    different doses. Subchronic administration of the drug mimicked the effects
    found after acute injection. The number of CARs in the extinction of
    shuttle-box active avoidance behavior appeared to be increased after acute
    IP or ICV injection, and after subchronic administration of
    acetyl-l-carnitine. The retention of passive avoidance behavior was
    facilitated by IP injection of the substance. The behavioral effects of
    acetyl-l-carnitine may involve central mechanisms, e.g., cholinergic
    neurotransmission in the brain.




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Fiore L; Rampello L.
\item [Title:]        L-acetylcarnitine attenuates the age-dependent decrease of
              NMDA-sensitive glutamate receptors in rat hippocampus.
\item [Language:]     English.

\item [Journal:]      Acta Neurologica, 1989 Oct, 11(5):346-50.

\item [CAS;EC No.:]   0 (N-methyl-D-aspartate receptor); 14992-62-2 (Acetylcarnitine);
              541-15-1 (Carnitine)

\item [Subject:]     *Acetylcarnitine -- pharmacology.
             *Aging -- metabolism.
              Animal.
             *Carnitine -- analogs \& derivatives.
              Hippocampus -- drug effects.
              Hippocampus -- growth \& development.
             *Hippocampus -- metabolism.
              Male.
              Rats.
              Rats, Inbred Strains.
              Support, Non-U.S. Gov't.
              Synaptic Receptors -- drug effects.
             *Synaptic Receptors -- physiology.

\item [Abstract:] NMDA-sensitive glutamate receptors are involved in the regulation of
    neuronal plasticity, and contribute to the synaptic mechanisms underlying
    the learning process. Aging is associated with a reduction in the maximal
    density of NMDA-sensitive glutamate binding sites in rat hippocampus. This
    reduction is attenuated after long-term administration with
    L-acetylcarnitine (10 mg/Kg i.p. once a day for 4 months). These results
    support a neuroprotective and neurotrophic role for L-acetylcarnitine
    during aging. 




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Guarnaschelli C; Fugazza G; Pistarini C.
\item [Address:]      Salvatore Maugeri Foundation, Work and Rehabilitation Clinic,
              IRCCS, Montescano (PV), Italy.
\item [Title:]        Pathological brain ageing: evaluation of the efficacy of a
              pharmacological aid.
\item [Language:]     English.

\item [Journal:]      Drugs under Experimental and Clinical Research, 1988,
             14(11):715-8.

\item [CAS;EC No.:]   14992-62-2 (Acetylcarnitine); 541-15-1 (Carnitine)

\item [Subject:]     *Acetylcarnitine -- therapeutic use.
              Aged.
              Aging.
             *Carnitine -- analogs \& derivatives.
              Female.
              Human.
              Male.
              Middle Age.
             *Organic Mental Disorders -- drug therapy.
              Organic Mental Disorders -- psychology.
              Psychiatric Status Rating Scales.
              Quality of Life.

\item [Abstract:] The efficacy of a molecule active at metabolic, neurotransmitter and
    membrane levels was evaluated in a group of 20 patients with typical
    involutional symptoms, who came under the care of the rehabilitation
    therapist for their concomitant decrease of motor activities. All subjects
    were treated with 1.5 g/day L-acetylcarnitine per os for 6 months, and
    subjected to the evaluation of cognitive ability (MMS), depression (HDRS),
    and behavioral and self-sufficiency performances (SCAG), at baseline (t0),
    after 90 days (t1), and after 180 days (t2). Whereas the basal evaluation
    showed disorders at all levels, the treatment gave a statistically
    significant improvement of all performances at both t1 and t2, achieving an
    effective recovery of the patients' quality of life, an improved
    participation in family and social life, and a diminished inertness in
    motor activity, which was the reason why they were studied.




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Ghirardi O; Milano S; Ramacci MT; Angelucci L.
\item [Address:]      Biological Research Laboratories, Sigma Tau S.p.A., Rome, Italy.
\item [Title:]        Long-term acetyl-L-carnitine preserves spatial learning in the
              senescent rat.
\item [Language:]     English.

\item [Journal:]      Progress in Neuro-Psychopharmacology and Biological Psychiatry,
             1989, 13(1-2):237-45.

\item [CAS;EC No.:]   14992-62-2 (Acetylcarnitine); 541-15-1 (Carnitine)

\item [Subject:]     *Acetylcarnitine -- pharmacology.
              Aging -- drug effects.
             *Aging -- psychology.
              Animal.
             *Avoidance Learning -- drug effects.
             *Carnitine -- analogs \& derivatives.
              Male.
              Rats.
              Rats, Inbred Strains.
              Swimming.

\item [Abstract:] 1. Untreated rats of different ages and old rats chronically treated
    with Acetyl-1-carnitine were subjected to the spatial learning task. 2. For
    this test, a circular pool filled with milk-opacified water was used. The
    animals were to reach an escape platform with the aid of visible
    environmental cues. 3. The experimental results indicated a clear-cut
    deterioration of the old animal's acquisition ability of a spatial learning
    task. 4. The long-term treatment (8 months) with Acetyl-1-carnitine was
    found to antagonize such a deterioration.




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Kohjimoto Y; Ogawa T; Matsumoto M; Shirakawa K; Kuwaki T; Yasuda
              H; Anami K; Fujii T; Satoh H; Ono T.
\item [Address:]      Research Laboratories, Fujisawa Pharmaceutical Co., Ltd., Osaka,
              Japan.
\item [Title:]        Effects of acetyl-L-carnitine on the brain lipofuscin content and
              emotional behavior in aged rats.
\item [Language:]     English.

\item [Journal:]      Japanese Journal of Pharmacology, 1988 Nov, 48(3):365-71.

\item [CAS;EC No.:]   14992-62-2 (Acetylcarnitine); 541-15-1 (Carnitine)

\item [Subject:]      Acetylcarnitine -- administration \& dosage.
             *Acetylcarnitine -- pharmacology.
              Aging -- metabolism.
              Aging -- psychology.
              Animal.
             *Behavior, Animal -- drug effects.
              Body Weight -- drug effects.
             *Brain -- drug effects.
              Brain -- metabolism.
             *Carnitine -- analogs \& derivatives.
              Histocytochemistry.
             *Lipofuscin -- metabolism.
              Male.
              Motor Activity -- drug effects.
             *Pigments -- metabolism.
              Rats.

\item [Abstract:] The effects of long-term dosing with acetyl-L-carnitine (ALC) were
    examined in aged rats, and they were compared with those in young rats. ALC
    significantly reduced the lipofuscin deposition in the brain of aged rats.
    Emotional parameters such as locomotor activity and rearing behavior are
    lower in aged rats than in young rats, and these behaviors decreased in
    both age groups during the experiments. ALC diminished the decrease of
    these emotional behaviors, especially in rearing behavior in the aged rats.
    Furthermore, ALC had no effect on body weight gain. These results might
    reflect one of the main beneficial pharmacological mechanisms of ALC in
    clinical use.




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Rai G; Wright G; Scott L; Beston B; Rest J; Exton-Smith AN.
\item [Address:]      Department of Geriatric Medicine, Whittington Hospital, London,
              England.
\item [Title:]        Double-blind, placebo controlled study of acetyl-l-carnitine in
              patients with Alzheimer's dementia.
\item [Language:]     English.

\item [Journal:]      Curr Med Res Opin, 1990, 11(10):638-47.

\item [CAS;EC No.:]   14992-62-2 (Acetylcarnitine); 541-15-1 (Carnitine)

\item [Subject:]      Acetylcarnitine -- adverse effects.
              Acetylcarnitine -- pharmacology.
             *Acetylcarnitine -- therapeutic use.
              Activities of Daily Living.
              Aged.
              Alzheimer's Disease -- diagnosis.
             *Alzheimer's Disease -- drug therapy.
              Alzheimer's Disease -- physiopathology.
             *Carnitine -- analogs \& derivatives.
              Double-Blind Method.
              Female.
              Human.
              Male.
              Memory, Short-Term -- drug effects.
              Randomized Controlled Trials.

\item [Abstract:] A randomized, double-blind, placebo-controlled, parallel-group
    clinical trial was carried out to compare 24-week periods of treatment with
    1 g acetyl-l-carnitine twice daily and placebo in the treatment of patients
    with dementia of the Alzheimer type. A total of 36 patients entered the
    trial, of whom 20 patients (7 active, 13 placebo) completed the full 24
    weeks. Whilst several of the efficacy indices showed little change in
    either group during the trial, there was an apparent trend for more
    improvement in the acetyl-l-carnitine group in relation to the Names
    Learning Test and a computerized Digit Recall Test, both related to aspects
    of short-term memory. Similarly, there was a trend for reaction time in the
    computerized classification test to show less deterioration in the active
    treatment group. Changes within groups, and changes between groups, failed
    to reach statistical significance, at least partially because of the small
    number of patients available for analysis. Two indices of overall
    therapeutic benefit showed a trend for less deterioration in the
    active-treatment group than in the placebo group. Nausea and/or vomiting
    occurred in 5 patients in the acetyl-l-carnitine group. Laboratory tests
    revealed no signs of drug toxicity. The results suggest that
    acetyl-l-carnitine may have a beneficial effect on some clinical features
    of Alzheimer-type dementia, particularly those related to short-term
    memory. 




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Tempesta E; Casella L; Pirrongelli C; Janiri L; Calvani M; Ancona
              L.
\item [Address:]      Department of Psychiatry and Psychology, Catholic University of
              the Sacred Heart, Rome, Italy.
\item [Title:]        L-acetylcarnitine in depressed elderly subjects. A cross-over
              study vs placebo.
\item [Language:]     English.

\item [Journal:]      Drugs under Experimental and Clinical Research, 1987,
             13(7):417-23.

\item [CAS;EC No.:]   14992-62-2 (Acetylcarnitine); 541-15-1 (Carnitine)

\item [Subject:]      Acetylcarnitine -- adverse effects.
             *Acetylcarnitine -- therapeutic use.
              Aged.
             *Carnitine -- analogs \& derivatives.
              Clinical Trials.
             *Depressive Disorder -- drug therapy.
              Depressive Disorder -- psychology.
              Female.
              Human.
              Male.
              Psychiatric Status Rating Scales.

\item [Abstract:] An open, cross-over study was performed on a population of 24
    geriatric patients hospitalized because of depressive syndrome. They were
    subdivided, according to Hamilton's Scale as modified for the aged, into
    low- and high-score subgroups. The study period covered 2 months. Half the
    patients received acetylcarnitine for 1 month and placebo thereafter (Group
    A); the other half received placebo and acetyl-carnitine thereafter (Group
   B). Statistical evaluation was twofold: parametrical analysis of variance
    was carried out on 4 subgroups (A1, A2, B1 and B2) and analysis of the
    score percentage modifications before and after treatment was performed on
    Groups A and B. The experimental results showed that acetylcarnitine
    treatment was highly effective and statistically significant in subgroups
    A1/B1, A2/B2, A1, B1 and B2. In particular, it should be noted that
    depressive tendencies were significantly modified in most groups, whereas
    general somatic symptoms as well as anxiety, asthenia and sleep
    disturbances proved to be little affected. Clinical evaluation, carried out
    by calculation of modifications in pre- and post-treatment score
    percentages, provided clear evidence that acetylcarnitine was particularly
    effective in patients showing more serious clinical symptoms. The drug
    caused no side-effects at the doses and regimens used.




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Baer RA.
\item [Address:]      Department of Psychology, University of Kentucky, Lexington
              40506-0044.
\item [Title:]        Effects of caffeine on classroom behavior, sustained attention,
              and a memory task in preschool children.
\item [Language:]     English.

\item [Journal:]      Journal of Applied Behavior Analysis, 1987 Fall, 20(3):225-34.

\item [CAS;EC No.:]   58-08-2 (Caffeine)

\item [Subject:]     *Attention -- drug effects.
             *Caffeine -- pharmacology.
              Carbonated Beverages -- adverse effects.
             *Child Behavior -- drug effects.
              Child, Preschool.
              Female.
              Human.
              Male.
             *Memory -- drug effects.
              Motor Activity -- drug effects.
              Paired-Associate Learning -- drug effects.
              Psychomotor Performance -- drug effects.
             *Recall -- drug effects.
             *Social Environment.

\item [Abstract:] The effects of caffeine on the behavior of young children is an
    important issue, as children in our society consume considerable amounts of
    caffeine, primarily in soft drinks. This study investigated the effects of
    normative amounts of caffeine on the behavior of 6 normal children in a
    kindergarten setting. Using a reversal design, counterbalanced for order of
    conditions, children's behavior was examined during a baseline condition, a
    caffeinated beverage condition, and a noncaffeinated beverage condition.
    Measures included direct observation of off-task and gross motor activity,
    actometer readings of movement, a Continuous Performance Test, a Paired
    Associates Learning Test, and teacher ratings of classroom behavior.
    Results suggest that caffeine exerts only small and inconsistent effects on
    the classroom behavior of kindergarten children. These results cast doubt
    on the importance of caffeine as a variable controlling the classroom
    behavior of normal kindergartners.




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Foreman N; Barraclough S; Moore C; Mehta A; Madon M.
\item [Address:]      Department of Psychology, University of Leicester, UK.
\item [Title:]        High doses of caffeine impair performance of a numerical version
              of the Stroop task in men.
\item [Language:]     English.

\item [Journal:]      Pharmacology, Biochemistry and Behavior, 1989 Feb, 32(2):399-403.

\item [CAS;EC No.:]   58-08-2 (Caffeine)

\item [Subject:]      Adult.
             *Caffeine -- pharmacology.
              Cognition -- drug effects.
              Human.
              Male.
              Memory, Short-Term -- drug effects.
             *Psychomotor Performance -- drug effects.
              Reaction Time -- drug effects.

\item [Abstract:] The effects of caffeine ingestion on mid-morning cognitive
    performance were investigated in thirty-two male subjects. These were given
   drinks containing either no caffeine, 125 mg caffeine (mean dose: 1.38
   mg/kg), or 250 mg caffeine (mean dose: 3.45 mg/kg) and were tested on three
   tasks: 1) free recall of supraspan word lists, 2) a response time
    (pointing) task and 3) a numerical Stroop task. There were no significant
    group differences on the recall task or in response times, but subjects
    having the higher caffeine dose were seriously impaired on the Stroop test,
    making particularly slow responses. Caffeine may have a deleterious effect
    on the rapid processing of ambiguous or confusing stimuli, and this may
    account for its clear effect on the Stroop test than on other cognitive
    tests used hitherto.




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Terry WS; Phifer B.
\item [Title:]        Caffeine and memory performance on the AVLT.
\item [Language:]     English.

\item [Journal:]      Journal of Clinical Psychology, 1986 Nov, 42(6):860-3.

\item [CAS;EC No.:]   58-08-2 (Caffeine)

\item [Subject:]      Adolescence.
              Adult.
             *Caffeine -- pharmacology.
              Depression, Chemical.
              Female.
              Human.
              Male.
             *Memory -- drug effects.
              Memory, Short-Term -- drug effects.
              Personality.
              Verbal Behavior -- drug effects.

\item [Abstract:] The Auditory-Verbal Learning Test (AVLT) is a memory test that
    assesses recall of lists of words on single and multiple trials. College
    students (N = 33) were given the AVLT, either with or without a prior
    administration of 100 mg caffeine. Caffeine subjects recalled fewer words
    than did control subjects, both after single presentations of lists and
    across repeated trials. Caffeine subjects showed a greater deficit in
    recalling the middle-to-end portions of the lists. Personality scores on
    the Maudsley Personality Inventory showed a positive correlation of recall
    on a pretest with Neuroticism, and no correlation with Introversion.




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Bologa L; Sharma J; Roberts E.
\item [Title:]        Dehydroepiandrosterone and its sulfated derivative reduce
              neuronal death and enhance astrocytic differentiation in brain
              cell cultures.
\item [Language:]     English.

\item [Journal:]      Journal of Neuroscience Research, 1987, 17(3):225-34.

\item [CAS;EC No.:]   53-43-0 (Dehydroepiandrosterone); 651-48-9
              (dehydroepiandrosterone sulfate)

\item [Subject:]      Animal.
             *Astrocytes -- drug effects.
             *Brain -- drug effects.
              Cell Differentiation -- drug effects.
              Cell Survival -- drug effects.
              Cells, Cultured.
              Comparative Study.
              Dehydroepiandrosterone -- analogs \& derivatives.
             *Dehydroepiandrosterone -- pharmacology.
              Embryo.
              Glial Fibrillary Acidic Protein -- metabolism.
              Intermediate Filament Proteins -- metabolism.
              Mice.
              Neurons -- drug effects.
              Support, Non-U.S. Gov't.
              Support, U.S. Gov't, P.H.S.

\item [Abstract:] Human studies of dehydroepiandrosterone (DHEA) and
    dehydroepiandrosterone sulfate (DHEA-S) have shown age-related changes in
    serum levels of these two sex hormone precursors. The levels of both DHEA
    and DHEA-S are characterized by monotonic decreases after puberty in
    females and after 20-24 yr of age in males. Further studies have shown that
    DHEA and DHEA-S levels are significantly low or close to minimal at ages
    when the incidence of senile dementia of Alzheimer's type (SDAT) begins to
    increase. We propose that DHEA and DHEA-S play a significant role in normal
    function of neuronal cells and that supplementation with them may prevent
    neuronal loss and/or damage. In the present study, using methods of
    immunocytochemistry, autoradiography, and scanning electron microscopy, we
    show that a supplement of as little as 10(-8) M DHEA or DHEA-S greatly
    increases neuronal survival and differentiation and reduces astroglial
    proliferation rates in mouse brain cells in cultures. These results suggest
    that correcting the DHEA and the DHEA-S deficit may prevent and/or improve
    the SDAT condition in humans.




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Cleary MP; Zisk JF.
\item [Title:]        Anti-obesity effect of two different levels of
              dehydroepiandrosterone in lean and obese middle-aged female
              Zucker rats.
\item [Language:]     English.

\item [Journal:]      International Journal of Obesity, 1986, 10(3):193-204.

\item [CAS;EC No.:]   EC 1.1.1.37 (Malate Dehydrogenase); EC 1.1.1.49 (Glucosephosphate
              Dehydrogenase); EC 6.- (Fatty Acid Synthetase Complex); 53-43-0
              (Dehydroepiandrosterone)

\item [Subject:]      Adipose Tissue -- drug effects.
              Animal.
             *Dehydroepiandrosterone -- therapeutic use.
              Dose-Response Relationship, Drug.
              Eating -- drug effects.
              Fatty Acid Synthetase Complex -- metabolism.
              Female.
              Glucosephosphate Dehydrogenase -- metabolism.
              Liver -- drug effects.
              Malate Dehydrogenase -- metabolism.
              Obesity -- blood.
             *Obesity -- drug therapy.
              Rats.
              Rats, Zucker.
              Support, Non-U.S. Gov't.

\item [Abstract:] Dehydroepiandrosterone has previously been shown to prevent weight
    gain in growing lean and obese mice and rats. In the present study, lean
    and obese female Zucker rats were treated with either 0.6 or 1.0 percent
    DHEA in the diet from 8 until 14 months of age. In lean rats, 0.6 percent
    DHEA prevented weight gain and 1.0 percent DHEA resulted in significant
    weight loss compared to initial body weight. Control lean rats had a
    significant weight gain. Both 0.6 and 1.0 percent DHEA obese rats lost
    weight over the experimental period while control obese rats gained weight.
    Food intake of DHEA-treated obese rats was lowered compared to control
    obese rats but was similar to that of all lean groups. DHEA lowered serum
    insulin levels in both lean and obese rats relative to control groups. Both
    0.6 and 1.0 percent DHEA lean rats had elevated hepatic G6PD activity
    compared to control lean rats. DHEA obese rats had lowered G6PD activity
    compared to the control obese rats. Hepatic malic enzyme was elevated by
    DHEA treatment in both lean and obese Zucker rats. Adipose tissue weights
    were lowered substantially in DHEA treated lean and obese rats versus their
    control groups. These data indicate that DHEA treatment in adult rats has
    an anti-obesity effect.




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Flood JF; Roberts E.
\item [Address:]      Geriatric Research, Education and Clinical Center (GRECC),
              Veterans Administration Hospital, Sepulveda, CA 91343.
\item [Title:]        Dehydroepiandrosterone sulfate improves memory in aging mice.
\item [Language:]     English.

\item [Journal:]      Brain Research, 1988 May 10, 448(1):178-81.

\item [CAS;EC No.:]   53-43-0 (Dehydroepiandrosterone); 651-48-9
              (dehydroepiandrosterone sulfate)

\item [Subject:]      Aging.
              Animal.
              Avoidance Learning -- drug effects.
             *Dehydroepiandrosterone -- analogs \& derivatives.
              Dehydroepiandrosterone -- pharmacology.
              Male.
             *Memory -- drug effects.
              Mice.
              Mice, Inbred C57BL.
              Support, Non-U.S. Gov't.
              Support, U.S. Gov't, Non-P.H.S.
              Support, U.S. Gov't, P.H.S.

\item [Abstract:] Middle-aged (18 month old) and old (24 month old) mice showed poorer
    retention of footshock active avoidance training (FAAT) than young mice (2
    month old). Immediate post-training subcutaneous injection of
    dehydroepiandrosterone sulfate (DHEAS) improved retention of FAAT in
    middle-aged and old mice to the high levels observed in young mice. DHEAS,
    a major naturally occurring adrenal steroid that decreases in blood serum
    with age, could be rate-limiting in achievement of retention of learning.




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Flood JF; Smith GE; Roberts E.
\item [Address:]      Psychobiology Research Laboratory, Veterans Administration
              Hospital, Sepulveda, CA 91343.
\item [Title:]        Dehydroepiandrosterone and its sulfate enhance memory retention
              in mice.
\item [Language:]     English.

\item [Journal:]      Brain Research, 1988 May 3, 447(2):269-78.

\item [CAS;EC No.:]   53-43-0 (Dehydroepiandrosterone); 651-48-9
              (dehydroepiandrosterone sulfate)

\item [Subject:]      Administration, Oral.
              Animal.
             *Dehydroepiandrosterone -- analogs \& derivatives.
              Dehydroepiandrosterone -- administration \& dosage.
             *Dehydroepiandrosterone -- pharmacology.
              Injections, Intraventricular.
              Injections, Subcutaneous.
              Male.
             *Memory -- drug effects.
              Mice.
             *Retention (Psychology) -- drug effects.
              Support, Non-U.S. Gov't.
              Support, U.S. Gov't, Non-P.H.S.

\item [Abstract:] Dehydroepiandrosterone (DHEA) and its sulfate (DHEAS), major
    naturally occurring precursors of both androgenic and estrogenic steroids,
    were shown in the present study to have convincing memory enhancing effects
    in mice. Post-training intracerebroventricular (i.c.v.) administration of
    DHEA in dimethylsulfoxide (2 microliters) prevented the amnesia for
    footshock active avoidance training (FAAT) caused by the same volume of
    dimethylsulfoxide alone. DHEAS significantly enhanced retention of FAAT in
    weakly trained mice whether injected i.c.v. or s.c. immediately
    post-training or given in the drinking water for a 2-week period. In the
    latter instance DHEAS was shown to facilitate retention of FAAT without
   enhancing acquisition. The maximally effective doses were: i.c.v., 162
    ng/mouse; s.c., 700 micrograms/mouse; and oral, 1.45 mg/mouse/day. DHEAS
    administered i.c.v. occluded the amnestic effects of anisomycin (inhibitor
    of protein synthesis) and scopolamine (muscarinic cholinergic antagonist).
    There was a time-dependence of the facilitatory effects of post-training
    i.c.v. administration of DHEAS on retention of FAAT, significant
    enhancement of retention being observed when it was given either
    immediately (within 2 min) or at 30 and 60 min after training, but not at
    90 or 120 min. DHEAS given i.c.v. also improved retention for step-down
    passive avoidance. In all instances, dose-dependent inverted U curves were
    obtained in a manner typical for memory enhancing substances. At a
    practical level, these experiments open new possibilities for the
    development of substances that may help in alleviating amnesic disorders in
    man.




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Mohan PF.
\item [Title:]        Dehydroepiandrosterone and Alzheimer's disease [letter].
\item [Language:]     English.

\item [Journal:]      Lancet, 1989 Oct 28, 2(8670):1048-9.

\item [CAS;EC No.:]   53-43-0 (Dehydroepiandrosterone)

\item [Subset:]       Abridged Index Medicus (AIM); Cancer Core journals.

\item [Subject:]     *Alzheimer's Disease -- drug therapy.
              Brain -- metabolism.
              Dehydroepiandrosterone -- metabolism.
             *Dehydroepiandrosterone -- therapeutic use.
              Human.
              Liver -- metabolism.





\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Roberts E; Bologa L; Flood JF; Smith GE.
\item [Title:]        Effects of dehydroepiandrosterone and its sulfate on brain tissue
              in culture and on memory in mice.
\item [Language:]     English.

\item [Journal:]      Brain Research, 1987 Mar 17, 406(1-2):357-62.

\item [CAS;EC No.:]   0 (neurofilament proteins); 53-43-0 (Dehydroepiandrosterone);
              651-48-9 (dehydroepiandrosterone sulfate)

\item [Subject:]      Animal.
              Avoidance Learning -- drug effects.
             *Brain -- drug effects.
              Cell Survival -- drug effects.
              Dehydroepiandrosterone -- analogs \& derivatives.
             *Dehydroepiandrosterone -- pharmacology.
              Embryo.
              Glial Fibrillary Acidic Protein -- metabolism.
              Intermediate Filament Proteins -- metabolism.
             *Memory -- drug effects.
              Mice.
              Support, Non-U.S. Gov't.
              Support, U.S. Gov't, Non-P.H.S.
              Tissue Culture.

\item [Abstract:] Low concentrations of dehydroepiandrosterone (DHEA) and
    dehydroepiandrosterone sulfate (DHEAS) enhanced neuronal and glial survival
    and/or differentiation in dissociated cultures of 14-day mouse embryo
    brain. Posttrial intracisternal injection into the brains of mice
    undergoing active avoidance training alleviated amnesia and enhanced
    long-term memory. By minimizing degenerative changes in injured nerve
    tissue and facilitating plastic changes, DHEA and DHEAS may be of use in
    treatment of neurodegenerative and memory disorders in man.




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Sunderland T; Merril CR; Harrington MG; Lawlor BA; Molchan SE;
              Martinez R; Murphy DL.
\item [Title:]        Reduced plasma dehydroepiandrosterone concentrations in
              Alzheimer's disease [letter].
\item [Language:]     English.

\item [Journal:]      Lancet, 1989 Sep 2, 2(8662):570.

\item [CAS;EC No.:]   53-43-0 (Dehydroepiandrosterone)

\item [Subset:]       Abridged Index Medicus (AIM); Cancer Core journals.

\item [Subject:]      Age Factors.
              Aged.
             *Alzheimer's Disease -- blood.
              Comparative Study.
             *Dehydroepiandrosterone -- blood.
              Evaluation Studies.
              Female.
              Human.
              Male.
              Middle Age.





\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Svec F; Lopez A.
\item [Title:]        Antiglucocorticoid actions of dehydroepiandrosterone and low
              concentrations in Alzheimer's disease [letter].
\item [Language:]     English.

\item [Journal:]      Lancet, 1989 Dec 2, 2(8675):1335-6.

\item [CAS;EC No.:]   50-23-7 (Hydrocortisone); 53-43-0 (Dehydroepiandrosterone)

\item [Subset:]       Abridged Index Medicus (AIM); Cancer Core journals.

\item [Subject:]      Adult.
              Aged.
              Aged, 80 and over.
             *Alzheimer's Disease -- metabolism.
              Alzheimer's Disease -- physiopathology.
              Dehydroepiandrosterone -- analysis.
             *Dehydroepiandrosterone -- pharmacology.
              Female.
              Human.
             *Hydrocortisone -- antagonists \& inhibitors.
              Male.
              Middle Age.





\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Auguet M; Delaflotte S; Hellegouarch A; Clostre F.
\item [Title:]        Bases pharmacologiques de l'impact vasculaire de l'extrait de
              Ginkgo biloba.
              [Pharmacological bases of the vascular impact of Ginkgo biloba
              extract].
\item [Language:]     French.

\item [Journal:]      Presse Medicale, 1986 Sep 25, 15(31):1524-8.

\item [References:]   33 (review article)

\item [Subset:]       Cancer Core journals.

\item [Subject:]      Animal.
             *Aorta -- drug effects.
              Dose-Response Relationship, Drug.
              Endothelium -- drug effects.
              English Abstract.
              In Vitro.
              Muscle Contraction -- drug effects.
              Muscle, Smooth, Vascular -- drug effects.
              Plant Extracts -- pharmacology.
             *Plants, Medicinal.
              Rabbits.
              Review.
             *Trees.
             *Venae Cavae -- drug effects.

\item [Abstract:] The preferential tissue irrigatory effect of Ginkgo biloba extract in
    ischaemic areas is largely explained by the direct impact of this product
    on both arteries and veins. The adrenergic vasoregulatory system and the
    vascular endothelium are the preferential targets for arterial impact.
    Ginkgo biloba extract reinforces the physiological vasoregulation of the
    sympathetic nervous system directly, by acting on neuromediator release,
    and indirectly, by inhibiting their extraneuronal degradation by
    catechol-orthomethyltransferase (C.O.M.T.) In the arterial endothelium
    Ginkgo biloba extract stimulates the release of endogenous relaxing
    factors, such as endothelium-derived relaxing factor, (EDRF) and
    prostacyclin. The action of Ginkgo biloba extract on the venous system has
    been shown to have a venoconstrictor component that maintains the degree of
    parietal tonus essential to the dynamic clearing of toxic metabolites
    accumulated during tissue ischaemia. The originality of the vascular impact
    mechanisms of Ginkgo biloba extract is due to the fact that the product can
    at the same time combat the phenomena resulting from vascular spasm and
    with the same efficiency restore circulation in areas subject to vasomotor
    paralysis.




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Funfgeld EW.
\item [Address:]      Faculty of the University of Marburg, FRG.
\item [Title:]        A natural and broad spectrum nootropic substance for treatment of
              SDAT--the Ginkgo biloba extract.
\item [Language:]     English.

\item [Journal:]      Progress in Clinical and Biological Research, 1989, 317:1247-60.

\item [Subject:]      Aged.
             *Alzheimer's Disease -- drug therapy.
              Alzheimer's Disease -- physiopathology.
              Case Report.
              Electroencephalography.
              Female.
              Human.
              Male.
              Middle Age.
             *Parkinson Disease -- drug therapy.
              Parkinson Disease -- physiopathology.
             *Plant Extracts -- therapeutic use.

\item [Abstract:] The efficacy of the Ginkgo biloba extract was not only found
    clinically or in standardised ratings but also documented by objective
    data, obtained by a computerized EEG method, the DYNAMIC BRAIN MAPPING and
    BRAIN FUNCTION MONITORING SYSTEM (Dr. T. Itil, New York). A one year open
    trial comprise 25 parkinson patients with additional signs of SDAT. Data
   from 3 selected cases were given: The short time efficacy of the substance
    after the infusion and the long-term result after the oral medication. The
    maps showed less slower and more faster waves. Without any side effects the
    Ginkgo biloba extract seems to be a substance with a broad spectrum of
    influence. Our therapeutic findings in parkinsonian patients with SDAT and
    the data taken from healthy elderly volunteers revealed that the
   computerized EEG method may have another big advantage: It seems that the
    so-called anteriorisation of the Theta waves can be taken as a preclinical
    sign of an incipient change in brain metabolism. As a consequence--it might
    be that these changes are reversible by an adequate nootropic treatment.
    Further studies and treatment experiences must confirm these preliminary
    findings. 




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Hindmarch I.
\item [Title:]        Activite de l'extrait de Ginkgo biloba sur la memoire a court
              terme.
              [Activity of Ginkgo biloba extract on short-term memory].
\item [Language:]     French.

\item [Journal:]      Presse Medicale, 1986 Sep 25, 15(31):1592-4.

\item [Subset:]       Cancer Core journals.

\item [Subject:]      Adult.
              Comparative Study.
              Dose-Response Relationship, Drug.
              Double-Blind Method.
              Drug Evaluation.
              English Abstract.
              Female.
              Human.
             *Memory, Short-Term -- drug effects.
              Plant Extracts -- pharmacology.
             *Plants, Medicinal.
              Psychological Tests.
              Reaction Time -- drug effects.
             *Trees.

\item [Abstract:] Eight healthy female volunteers were included in a double-blind,
    cross-over trial comparing Ginkgo biloba extract in acute and ascending
    doses (120, 240, 600 mg) with a placebo. One hour after treatment they were
   subjected to a battery of tests, including: critical flicker fusion, choice
    reaction time, subjective rating scale and Sternberg memory scanning test.
    No statistically significant differences with the placebo were observed in
    the first three tests. In contrast, short term memory, as assessed by the
    Sternberg technique, was very significantly improved following 600 mg of
    Ginkgo biloba extract, as compared with the placebo. These results
    differentiate Ginkgo biloba extract from sedative and stimulant drugs and
    suggest a specific effect on memory processes.




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Allard M.
\item [Title:]        Traitement des troubles du vieillissement par extrait de Ginkgo
              biloba. De la pharmacologie a la clinique.
              [Treatment of the disorders of aging with Ginkgo biloba extract.
              From pharmacology to clinical medicine].
\item [Language:]     French.

\item [Journal:]      Presse Medicale, 1986 Sep 25, 15(31):1540-5.

\item [References:]   38 (review article)

\item [Subset:]       Cancer Core journals.

\item [Subject:]     *Aging -- drug effects.
              Alzheimer's Disease -- drug therapy.
              Alzheimer's Disease -- metabolism.
              Brain -- drug effects.
              Brain -- metabolism.
              Cerebral Ischemia -- drug therapy.
              Cerebral Ischemia -- metabolism.
              Cerebrovascular Circulation -- drug effects.
              English Abstract.
              Free Radicals.
              Human.
              Neural Transmission -- drug effects.
              Neurons -- drug effects.
              Neurons -- metabolism.
              Plant Extracts -- pharmacology.
              Plant Extracts -- therapeutic use.
             *Plants, Medicinal.
              Review.
             *Trees.

\item [Abstract:] Ginkgo biloba extract is prescribed in psychic and behavioural
    disorders of the elderly, in peripheral vascular deficiency and in
    functional disorders of ischaemic origin in the E.N.T. and eye areas.
    Numerous controlled clinical trials justify these prescriptions and are in
    agreement with the pharmacological data currently available.
    Experimentally, Ginkgo biloba extract has proved active on the circulatory
    and rheological functions, on neuronal metabolism threatened by ischaemia
    or hypoxia, on neurotransmission and on membrane lesions caused by free
    oxygenated radicals. Concerning Alzheimer's disease and dementia, no firm
    conclusion can be drawn for the time being due to the lack of animal model.
    However, experimental data suggest that the product may act on a number of
    major elements of these diseases. From what is already known about Ginkgo
    biloba extract, it appears that it fulfills the conditions laid down by the
    W.H.O. concerning the development of drugs effective against cerebral
    ageing.




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Taillandier J; Ammar A; Rabourdin JP; Ribeyre JP; Pichon J;
              Niddam S; Pierart H.
\item [Title:]        Traitement des troubles du vieillissement cerebral par l'extrait
              de Ginkgo biloba. Etude longitudinale multicentrique a double
              insu face au placebo.
              [Treatment of cerebral aging disorders with Ginkgo biloba
              extract. A longitudinal multicenter double-blind drug vs. placebo
              study].
\item [Language:]     French.

\item [Journal:]      Presse Medicale, 1986 Sep 25, 15(31):1583-7.

\item [Subset:]       Cancer Core journals.

\item [Subject:]      Aged.
              Aged, 80 and over.
             *Aging -- drug effects.
             *Brain Diseases -- drug therapy.
              Brain Diseases -- etiology.
              Clinical Trials.
              Comparative Study.
              Double-Blind Method.
              English Abstract.
              Female.
              Human.
              Longitudinal Studies.
              Male.
              Middle Age.
              Placebos.
              Plant Extracts -- therapeutic use.
             *Plants, Medicinal.
              Time Factors.
             *Trees.

\item [Abstract:] The effectiveness of Ginkgo biloba extract in the treatment of
    cerebral disorders due to ageing was evaluated in a multicentric,
    double-blind, drug versus placebo trial involving 166 patients. In this
    study carried out under strict methodological conditions a specially
    devised geriatric clinical evaluation scale was used. The results confirmed
    that Ginkgo biloba extract is effective against cerebral disorders due to
    ageing. The difference between control and treatment groups became
    significant at 3 months and increased during the following months. These
    results were concordant with the overall clinical assessment made by the
    specialist in charge.




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Warburton DM.
\item [Title:]        Psycho-pharmacologie clinique de l'extrait de Ginkgo biloba.
              [Clinical psychopharmacology of Ginkgo biloba extract].
\item [Language:]     French.

\item [Journal:]      Presse Medicale, 1986 Sep 25, 15(31):1595-604.

\item [References:]   30 (review article)

\item [Subset:]       Cancer Core journals.

\item [Subject:]      Aging -- drug effects.
              Brain -- drug effects.
              Brain -- physiology.
              Cerebrovascular Circulation -- drug effects.
              Drug Evaluation -- methods.
              Drug Tolerance.
              Electroencephalography.
              English Abstract.
              Human.
              Neurons -- drug effects.
              Neurons -- metabolism.
              Plant Extracts -- administration \& dosage.
              Plant Extracts -- pharmacology.
             *Plants, Medicinal.
              Psychological Tests.
              Psychometrics.
              Psychopharmacology.
              Review.
             *Trees.

\item [Abstract:] From this general review of the pharmacological,
    psychopharmacological and clinical studies performed with Ginkgo biloba
   extract, the following conclusions can be drawn: the drug seems to be
    effective in patients with vascular disorders, in all types of dementia and
    even in patients suffering from cognitive disorders secondary to
    depression, because of its beneficial effects on mood. Of special concern
    are people who are just beginning to experience deterioration in their
    cognitive function. Ginkgo biloba extract might delay deterioration and
    enable these subject to maintain a normal life and escape
    institutionalization. In addition, Ginkgo biloba extract appears to be a
    safe drug, being well tolerated, even in doses many times higher than those
    usually recommended.




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Petkov VD; Mosharrof AH.
\item [Address:]      Institute of Physiology, Bulgarian Academy of Sciences, Sofia.
\item [Title:]        Effects of standardized ginseng extract on learning, memory and
              physical capabilities.
\item [Language:]     English.

\item [Journal:]      American Journal of Chinese Medicine, 1987, 15(1-2):19-29.

\item [Subject:]      Animal.
              Conditioning (Psychology) -- drug effects.
              Dose-Response Relationship, Drug.
              Drugs, Chinese Herbal -- administration \& dosage.
             *Drugs, Chinese Herbal -- pharmacology.
             *Ginseng.
             *Learning -- drug effects.
              Male.
             *Memory -- drug effects.
             *Motor Activity -- drug effects.
              Rats.
              Rats, Inbred Strains.

\item [Abstract:] Standardized ginseng extract (G115, Pharmaton, Lugano) was
    administered orally at doses of 3, 10, 30, 100 and 300 mg/kg for 10 days as
    ten rats were used with each dose. With the "shuttle-box" method for active
    avoidance most pronounced effect on learning and memory was obtained by the
    dose of 10 mg/kg. With the "step-down" method for passive avoidance the
    dose of 30 mg/kg significantly improved retention. In the staircase maze
    training with positive (alimentary) reinforcement only the dose of 10 mg/kg
    significantly improved learning and memory. The dose of 100 mg/kg greatly
    increased the locomotor activity of mice. The results show that ginseng at
    appropriate doses improves learning, memory and physical capabilities.
    Bell-shaped dose-effect curves, reported with other nootropic drugs, were
    obtained.




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Kawakami M; Itoh T.
\item [Address:]      3rd Department of Internal Medicine, St. Marianna University
              School of Medicine, Kawasaki, Japan.
\item [Title:]        Effects of idebenone on monoamine metabolites in cerebrospinal
              fluid of patients with cerebrovascular dementia.
\item [Language:]     English.

\item [Journal:]      Arch Gerontol Geriatr, 1989 May, 8(3):343-53.

\item [CAS;EC No.:]   1321-73-9 (Hydroxyindoleacetic Acid); 306-08-1 (Homovanillic
              Acid); 534-82-7 (Methoxyhydroxyphenylglycol); 58186-27-9 (CV
              2619)

\item [Subject:]      Aged.
              Aged, 80 and over.
             *Biogenic Monoamines -- cerebrospinal fluid.
              Biogenic Monoamines -- metabolism.
             *Dementia, Vascular -- cerebrospinal fluid.
              Dementia, Vascular -- drug therapy.
              Dementia, Vascular -- metabolism.
              Homovanillic Acid -- cerebrospinal fluid.
              Human.
              Hydroxyindoleacetic Acid -- cerebrospinal fluid.
              Male.
              Methoxyhydroxyphenylglycol -- cerebrospinal fluid.
              Middle Age.
             *Quinones -- pharmacology.

\item [Abstract:] Monoamine metabolites and norepinephrine (NE) in the cerebrospinal
    fluid of patients with cerebrovascular dementia were measured to study the
    effects of administration of idebenone. Six patients with cerebral
    infarction and one with cerebral hemorrhage (mean age 65.4 years) were
    enrolled as subjects. All the patients had mental and intelligence
    impairment which was evaluated by the Hasegawa's Dementia Rating (DR)
    Scale. The patients were medicated with a 90 mg/day dose of idebenone for 1
    to 2 months, and homovanillic acid (HVA), 5-hydroxyindole acetic acid
    (5-HIAA), 3-methoxy-4-hydroxyphenylethyleneglycol (MHPG) and NE in the
    cerebrospinal fluid were determined by high-performance liquid
    chromatography before and after the medication of idebenone. Before the
    medication, the level of HVA was 21.7 +/- 1.4 ng/ml (mean +/- SE), which
    was significantly lower (p less than 0.01) as compared with that in control
    subjects of similar age. The level of 5-HIAA was 18.5 +/- 2.7 ng/ml, and
    that of MHPG 9.5 +/- 0.7 ng/ml, both of which were lower than those of the
    controls, though statistically not significant. NE was similar to the
    control value. After administration of idebenone, HVA measured was 27.1 +/-
    3.2 ng/ml, showing a tendency to increase. The levels of 5-HIAA and MHPG
    were 26.7 +/- 2.3 ng/ml and 10.7 +/- 0.6 ng/ml, respectively, which were
    significantly (p less than 0.05) higher than the premedication values. The
    percentages of the change were 12.8 +/- 8.0 for HVA, 58.2 +/- 18.5 for
    5-HIAA and 14.2 +/- 5.0 for MHPG. The score of the DR scale was improved by
    5 or less after the idebenone medication in most subjects. HVA and 5-HIAA
    increased markedly in the patients who showed a tendency of improvement of
    mental impairment as evaluated by the DR scale. The results suggested that
    idebenone would improve abnormalities in neurotransmitters of patients with
    cerebrovascular dementia, especially promoting serotonin turnover.





\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Kawakami M; Itoh T.
\item [Title:]        [Effects of idebenone on monoamine metabolites in the
              cerebrospinal fluid of patients with cerebrovascular dementia].
\item [Language:]     Japanese.

\item [Journal:]      No To Shinkei. Brain and Nerve, 1986 Feb, 38(2):187-93.

\item [CAS;EC No.:]   1321-73-9 (Hydroxyindoleacetic Acid); 306-08-1 (Homovanillic
              Acid); 51-41-2 (Norepinephrine); 534-82-7
              (Methoxyhydroxyphenylglycol); 58186-27-9 (CV 2619)

\item [Subject:]      Aged.
             *Biogenic Amines -- metabolism.
             *Cerebrovascular Disorders -- cerebrospinal fluid.
              Cerebrovascular Disorders -- drug therapy.
              Chromatography, High Pressure Liquid.
             *Dementia -- cerebrospinal fluid.
              Dementia -- drug therapy.
              Dementia, Senile -- cerebrospinal fluid.
              Dementia, Senile -- drug therapy.
              English Abstract.
              Homovanillic Acid -- cerebrospinal fluid.
              Human.
              Hydroxyindoleacetic Acid -- cerebrospinal fluid.
              Methoxyhydroxyphenylglycol -- cerebrospinal fluid.
              Middle Age.
              Norepinephrine -- cerebrospinal fluid.
             *Quinones -- therapeutic use.

\item [Abstract:] Elucidation of the alterations of intracerebral neurotransmitters in
    cerebrovascular dementia is of prime importance not only in revealing
    patho-physiological mechanism but also in developing the therapy for the
    disease. We measured monoamine metabolites and norepinephrine (NE) in
    cerebrospinal fluid of patients with cerebrovascular dementia, to study the
    effects of administration of 6-(10-hydroxydecyl)-2,
    3-dimethoxy-5-metyl-1,4-benzoquinone (idebenone, CV-2619). Six patients
    with cerebral infarction and 1 with cerebral hemorrhage, at the mean age of
    65.4 years, were enrolled as subjects. All patients had mental and
    intelligent impairment, and the Hasegawa's Dementia Rating (DR) Scale was
    performed. The patients were medicated with 90 mg daily dose of CV-2619 for
    1 to 2 months, and homovanillic acid (HVA), 5-hydroxyindole acetic acid
    (5-HIAA), 3-methoxy-4-hydroxyphenylethylenglycol (MHPG), NE in
    cerebrospinal fluid were determined by high-performance liquid
    chromatography before and also after the medication. Before the medication,
    HVA was 21.7 +/- 1.4 ng/ml (mean +/- SE), which was significantly low (p
   less than 0.01), compared with controls at a similar age: 5-HIAA was 18.5
    +/- 2.7 ng/ml, and MHPG, 9.5 +/- 0.7 ng/ml, both of which were not
    significantly low, but tended to be low, compared with the controls. NE was
    similar to the control value. With the administration of CV-2619, HVA
    measured 27.1 +/- 3.2 ng/ml, showing a tendency to increase; 5-HIAA was
    26.7 +/- 2.3 ng/ml, and MHPG, 10.7 +/- 0.6 ng/ml, both of which increased
    significantly (p less than 0.05), compared with the respective
    premedication values.(ABSTRACT TRUNCATED AT 250 WORDS)




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Kiyota Y; Miyamoto M; Nagaoka A.
\item [Address:]      Central Research Division, Takeda Chemical Industries, Ltd.,
              Osaka, Japan.
\item [Title:]        [Ameliorating effects of idebenone and indeloxazine hydrochloride
              on impairment of radial maze learning in cerebral embolized
              rats].
\item [Language:]     Japanese.

\item [Journal:]      Nippon Yakurigaku Zasshi. Folia Pharmacologica Japonica, 1989
             Mar, 93(3):197-202.

\item [CAS;EC No.:]   58186-27-9 (CV 2619); 60929-23-9 (indeloxazine)

\item [Subject:]      Animal.
             *Antidepressive Agents -- therapeutic use.
             *Cerebral Embolism and Thrombosis -- complications.
              English Abstract.
             *Learning Disorders -- drug therapy.
              Learning Disorders -- etiology.
              Male.
             *Memory Disorders -- drug therapy.
              Memory Disorders -- etiology.
             *Morpholines -- therapeutic use.
             *Quinones -- therapeutic use.
              Rats.
              Rats, Inbred Strains.

\item [Abstract:] The ameliorating effects of idebenone and indeloxazine hydrochloride
    on the impairment of memory and learning were studied in cerebral embolized
    rats. The embolized rats had impaired memory and learning ability in the
    radial maze task; these were demonstrated by a decrease in correct
    responses and an increase in total errors. In particular, the rats showed
    severe impairment of working memory, as shown by a marked increase in the
    numbers of re-entries into the arm that had been already visited. Idebenone
    (30 mg/kg, p.o.) exerted marked ameliorating effects on the impairment in
   the embolized rats: the drug significantly increased the correct responses
    and decreased the errors. Indeloxazine hydrochloride also improved the
    memory impairment in the embolized rats, as shown by a reduction of the
    errors. The ameliorating effects of these drugs may be due mainly to
    improvement of hypofunctions of the central nervous system. These results
    confirm that idebenone and indeloxazine hydrochloride may have ameliorating
    actions on impairment of memory and learning induced by brain hypofunction,
    and they suggest that the action of idebenone is more potent than that of
    indeloxazine hydrochloride.




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Suno M; Nagaoka A.
\item [Address:]      Central Research Division, Takeda Chemical Industries, Ltd.,
              Osaka, Japan.
\item [Title:]        [Effect of idebenone and various nootropic drugs on lipid
              peroxidation in rat brain homogenate in the presence of
              succinate].
\item [Language:]     Japanese.

\item [Journal:]      Nippon Yakurigaku Zasshi. Folia Pharmacologica Japonica, 1988
             May, 91(5):295-9.

\item [CAS;EC No.:]   1977-33-9 (pantogab); 42971-12-0 (ethyl apovincaminate); 56-12-2
              (GABA); 58186-27-9 (CV 2619); 60929-23-9 (indeloxazine);
              62232-46-6 (MCI 2016); 79-83-4 (Pantothenic Acid)

\item [Subject:]      Animal.
              Benzhydryl Compounds -- pharmacology.
             *Brain -- metabolism.
              Depression, Chemical.
              Dose-Response Relationship, Drug.
              English Abstract.
              GABA -- analogs \& derivatives.
              GABA -- pharmacology.
              In Vitro.
             *Lipid Peroxides -- biosynthesis.
              Male.
              Morpholines -- pharmacology.
              Pantothenic Acid -- analogs \& derivatives.
              Pantothenic Acid -- pharmacology.
             *Quinones -- pharmacology.
              Rats.
              Rats, Inbred Strains.
             *Succinates -- pharmacology.
              Vinca Alkaloids -- pharmacology.

\item [Abstract:] The effects of idebenone and various nootropic drugs on lipid
    peroxidation in rat brain homogenate were examined. Idebenone inhibited
    lipoperoxide (LPO) production in brain homogenate in a
    concentration-dependent manner, with an IC50 of 38 microM. The inhibition
    was strongly enhanced (about 100-fold) by adding succinate, a substrate in
    the mitochondrial respiration. The optimal concentration of succinate was
    0.5 mM. Inhibition of lipid peroxidation in brain homogenate by various
    nootropic drugs in the presence or absence of succinate was then examined.
    Drugs added to the brain homogenate at 100 microM in the absence of
   succinate inhibited LPO production in the order: idebenone greater than
    vinpocetine greater than bifemelane greater than indeloxazine greater than
    calcium hopantenate. However, when the drugs were added at 1 microM in the
    presence of succinate, only idebenone demonstrated inhibition. These
    results suggest that although almost all of the drugs tested inhibit lipid
    peroxidation in brain homogenate, only idebenone is activated by succinate,
    the other drugs being insensitive to this compound.




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Yamazaki N; Nomura M; Nagaoka A; Nagawa Y.
\item [Address:]      Central Research Division, Takeda Chemical Industries, Ltd.,
              Osaka, Japan.
\item [Title:]        Idebenone improves learning and memory impairment induced by
              cholinergic or serotonergic dysfunction in rats.
\item [Language:]     English.

\item [Journal:]      Arch Gerontol Geriatr, 1989 May, 8(3):225-39.

\item [CAS;EC No.:]   50-67-9 (Serotonin); 51-34-3 (Scopolamine); 51-84-3
              (Acetylcholine); 58186-27-9 (CV 2619)

\item [Subject:]     *Acetylcholine -- physiology.
              Animal.
              Cerebral Cortex -- drug effects.
             *Cerebrovascular Disorders -- complications.
             *Cerebrovascular Disorders -- physiopathology.
              Discrimination Learning -- drug effects.
             *Learning Disorders -- drug therapy.
              Male.
              Memory Disorders -- chemically induced.
             *Memory Disorders -- drug therapy.
              Memory, Short-Term -- drug effects.
              Quinones -- administration \& dosage.
             *Quinones -- pharmacology.
              Rats.
              Rats, Inbred Strains.
              Scopolamine.
             *Serotonin -- physiology.

\item [Abstract:] The effects of idebenone, a cerebral metabolic enhancer, on learning
    and memory impairment in two rat models with central cholinergic or
    serotonergic dysfunction were investigated using positively reinforced
    learning tasks. A delayed alternation task using a T maze was employed to
    test the effect of idebenone on short-term memory impairment induced by a
    cholinergic antagonist, scopolamine. A correct response, defined as a turn
    toward the arm opposite to that in the forced run, was rewarded with food
    pellets. Scopolamine (0.2 and 0.5 mg/kg, i.p.) significantly decreased the
    correct responses to the chance level in the 60-s-delayed alternation task.
    The scopolamine (0.2 mg/kg, i.p.)-induced impairment of short-term memory
    was improved by idebenone (3-30 mg/kg, i.p.) or an acetylcholinesterase
    inhibitor, physostigmine (0.1 and 0.2 mg/kg, i.p.), administered
    simultaneously. The central serotonergic dysfunction model was produced by
    giving rats a diet deficient in tryptophan, a precursor of serotonin. The
    rats fed on a tryptophan-deficient diet (TDD) showed a slower learning
    process in the operant brightness discrimination task (mult V115 EXT) than
    did rats fed on a normal diet. Idebenone (60 mg/kg/day) admixed with the
    TDD decreased the number of lever-pressing responses emitted during the
    extinction periods. The percentage of correct responses was significantly
    higher in the idebenone-treated group than in the control TDD group. These
    results suggest that idebenone may improve both the impairment of
    short-term memory induced by a decreased cholinergic activity and the
    retardation of discrimination learning induced by central serotonergic
    dysfunction.




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       DeNoble VJ; Repetti SJ; Gelpke LW; Wood LM; Keim KL.
\item [Title:]        Vinpocetine: nootropic effects on scopolamine-induced and
              hypoxia-induced retrieval deficits of a step-through passive
              avoidance response in rats.
\item [Language:]     English.

\item [Journal:]      Pharmacology, Biochemistry and Behavior, 1986 Apr, 24(4):1123-8.

\item [CAS;EC No.:]   11032-41-0 (Dihydroergotoxine); 1617-90-9 (Vincamine); 42971-12-0
              (ethyl apovincaminate); 51-34-3 (Scopolamine); 72432-10-1
              (aniracetam)

\item [Subject:]      Animal.
              Avoidance Learning.
              Cerebral Anoxia -- complications.
              Dihydroergotoxine -- therapeutic use.
              Male.
              Memory Disorders -- chemically induced.
             *Memory Disorders -- prevention \& control.
              Pyrrolidinones -- therapeutic use.
              Rats.
              Rats, Inbred Strains.
              Reaction Time.
              Scopolamine.
             *Vinca Alkaloids -- therapeutic use.
              Vincamine -- therapeutic use.

\item [Abstract:] Vinpocetine, vincamine, aniracetam, and Hydergine, compounds with
    purported cognition activating activity, were evaluated for their ability
    to prevent scopolamine-induced and hypoxia-induced impairment of passive
    avoidance retention (24 hr) in rats. Vinpocetine (peak effect dose [PED]=
    200 mg/kg PO), aniracetam (PED = 100 mg/kg PO), vincamine (PED = 30 mg/kg
    PO), and Hydergine (PED = 1 mg/kg PO) prevented memory disruption by
    scopolamine. Vinpocetine (PED = 3 mg/kg PO) and aniracetam (PED = 30 mg/kg
    PO) were also effective in preventing disruption of passive avoidance
    retention impaired by 7\% oxygen hypoxia. In contrast, Hydergine (0.05 to 3
    mg/kg PO) and vincamine (0.3 to 100 mg/kg PO) were not effective against
    hypoxia-induced impairment. Hydergine at doses greater than 10 mg/kg PO
    markedly impaired motor function. In both tests the protection was
    dose-related for all test substances in an inverted U-shaped manner.
    Mecamylamine (1, 3, 10 mg/kg SC), (-)-nicotine (0.1 to 0.4 mg/kg SC),
    apovincaminic acid (1-400 mg/kg PO) and pemoline (1-100 mg/kg PO) did not
    protect against memory impairment induced by either procedure. These data
    support the view that vinpocetine, a compound chemically distinct from the
    pyrrolidinones, has a cognitive activating ability as defined in models of
    both scopolamine-induced and hypoxia-induced memory impairment in rats.




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Domingo JL; Gomez M; Llobet JM; Corbella J.
\item [Address:]      Laboratory of Toxicology \& Biochemistry, School of Medicine,
              University of Barcelona, Reus, Spain.
\item [Title:]        Citric, malic and succinic acids as possible alternatives to
              deferoxamine in aluminum toxicity.
\item [Language:]     English.

\item [Journal:]      Journal of Toxicology. Clinical Toxicology, 1988, 26(1-2):67-79.

\item [CAS;EC No.:]   110-15-6 (succinic acid); 6915-15-7 (malic acid); 70-51-9
              (Deferoxamine); 7429-90-5 (Aluminum); 77-92-9 (citric acid)

\item [Subset:]       Abridged Index Medicus (AIM)

\item [Subject:]      Aluminum -- pharmacokinetics.
             *Aluminum -- toxicity.
              Animal.
              Brain Chemistry.
              Citrates -- administration \& dosage.
             *Citrates -- therapeutic use.
              Comparative Study.
             *Deferoxamine -- therapeutic use.
              Feces -- analysis.
              Injections, Intraperitoneal.
              Kidney -- analysis.
              Liver -- analysis.
              Malates -- administration \& dosage.
             *Malates -- therapeutic use.
              Male.
              Mice.
              Succinates -- administration \& dosage.
             *Succinates -- therapeutic use.
              Support, Non-U.S. Gov't.

\item [Abstract:] The effect of repeated intraperitoneal administration of
    deferoxamine, citric, malic and succinic acids on the distribution and
    excretion of aluminum was determined in male Swiss mice which had
    previously received aluminum nitrate intraperitoneally at a daily dose of
    0.27 mmol/kg for five weeks. Chelating agents were administered for two
    weeks at doses approximately equal to one-fourth of their respective LD50.
    Treatment with DFOA, citric, malic or succinic acids significantly
    increased the fecal and urinary excretion of aluminum and reduced the
    concentration of aluminum found in various organs and tissues, with citric
    acid being the most effective. In sight of these results, citric, malic or
    succinic acids may be considered as alternatives to deferoxamine in
    aluminum toxicity. However, further investigations are required previous to
    the possible use of these compounds in human aluminum poisoning.




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Martyn CN; Barker DJ; Osmond C; Harris EC; Edwardson JA; Lacey
              RF.
\item [Address:]      Medical Research Council Environmental Epidemiology Unit,
              Southampton General Hospital.
\item [Title:]        Geographical relation between Alzheimer's disease and aluminum in
              drinking water.
\item [Language:]     English.

\item [Journal:]      Lancet, 1989 Jan 14, 1(8629):59-62.

\item [CAS;EC No.:]   7429-90-5 (Aluminum)

\item [Subset:]       Abridged Index Medicus (AIM); Cancer Core journals.

\item [Subject:]      Adult.
              Age Factors.
              Aged.
              Aluminum -- adverse effects.
             *Aluminum -- analysis.
              Alzheimer's Disease -- chemically induced.
             *Alzheimer's Disease -- epidemiology.
              Alzheimer's Disease -- radiography.
              Comparative Study.
              Dementia -- epidemiology.
             *Drinking.
              England.
              Epidemiologic Methods.
              Epilepsy -- epidemiology.
              Female.
              Human.
              Male.
              Middle Age.
              Regression Analysis.
              Risk Factors.
              Tomography, X-Ray Computed.
              Wales.
             *Water Supply -- analysis.
              Water Supply -- standards.

\item [Abstract:] In a survey of eighty-eight county districts within England and
    Wales, rates of Alzheimer's disease in people under the age of 70 years
    were estimated from the records of the computerised tomographic (CT)
    scanning units that served these districts. Rates were adjusted to
    compensate for differences in distance from the nearest CT scanning unit
    and for differences in the size of the population served by the units.
    Aluminium concentrations in water over the past 10 years were obtained from
    water authorities and water companies. The risk of Alzheimer's disease was
    1.5 times higher in districts where the mean aluminium concentration
    exceeded 0.11 mg/l than in districts where concentrations were less than
    0.01 mg/l. There was no evidence of a relation between other causes of
    dementia, or epilepsy, and aluminium concentrations in water.




\end{list}

\section{}
\begin{list}{}{\settowidth{\labelwidth}{CAS;EC No.:\hspace*{1em}}}
\item [Author:]       Piccardo P; Yanagihara R; Garruto RM; Gibbs CJ Jr; Gajdusek DC.
\item [Address:]      Laboratory of Central Nervous System Studies, National Institutes
              of Health, Bethesda, MD 20892.
\item [Title:]        Histochemical and X-ray microanalytical localization of aluminum
              in amyotrophic lateral sclerosis and parkinsonism-dementia of
              Guam.
\item [Language:]     English.

\item [Journal:]      Acta Neuropathologica, 1988, 77(1):1-4.

\item [CAS;EC No.:]   480-16-0 (morin); 7429-90-5 (Aluminum)

\item [Subject:]      Adolescence.
              Adult.
              Aged.
             *Aluminum -- metabolism.
              Amyotrophic Lateral Sclerosis -- epidemiology.
             *Amyotrophic Lateral Sclerosis -- metabolism.
              Dementia -- epidemiology.
              Dementia -- etiology.
             *Dementia -- metabolism.
             *Electron Probe Microanalysis.
              Female.
              Flavones.
              Guam.
             *Histocytochemistry -- methods.
              Human.
              Male.
              Middle Age.
              Parkinson Disease -- complications.
              Parkinson Disease -- epidemiology.
             *Parkinson Disease -- metabolism.
              Stains and Staining.

\item [Abstract:] Histochemical staining for aluminum, using Solochrome azurine or
    Morin, provided a rapid, simple and reliable means of identifying areas and
    structures of the brain of interest for closer scrutiny by X-ray
    microanalysis in patients with amyotrophic lateral sclerosis and
    parkinsonism-dementia of Guam. Neuronal perikarya, dendritic processes, and
    the walls of some cerebral vessels were aluminum positive by Solochrome
    azurine staining. In some cases, the deposition of aluminum was rather
    diffuse, particularly in the white matter. Fluorescent localization of
    aluminum using Morin was equally sensitive and specific, but provided less
    morphological detail than Solochrome azurine. Confirmation of histochemical
    detection of aluminum was achieved by examining adjacent tissue sections
    using wavelength-dispersive spectrometry coupled to a computer-controlled
    electron beam X-ray microprobe. Although the minimum detectable limits for
    aluminum by these histochemical procedures are unknown, the lower detection
    limit of our X-ray microanalytical technique is 10-100 ppm dry weight.
    Solochrome and Morin staining, as verified by X-ray microanalysis, afford a
    useful and reliable means of surveying multiple anatomical regions for
    aluminum deposition in naturally occurring and experimentally induced
    neurodegenerative disorders.



\end{list}

\end{document}





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