In search of the mechanism of action of the nootropics: New insights and potential clinical implications

Mondadori, Cesare

doi:10.1016/0024-3205(94)00398-x

Cited by 21 publications

(16 citation statements)

References 51 publications

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“…Our present results further found that HBA reversed the CXM-induced impairment in sham and ADX rats but its effect in ADX rats was weaker than that in sham rats. The result of positive control PIR was consistent with another early report (Mondadori, 1994) that ADX blocked the ameliorating effect of PIR on CXM-induced impairment of passive avoidance response. On the other hand, we found that the pain threshold and motor activities of sham or ADX rats who received vehicle, HBA or PIR were grossly normal.…”

Section: Discussionsupporting

confidence: 90%

p-Hydroxybenzyl Alcohol, an Active Phenolic Ingredient of Gastrodia elata, Reverses the Cycloheximide-Induced Memory Deficit by Activating the Adrenal Gland in Rats

Chen

Tsai

et al. 2015

Am. J. Chin. Med.

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The present study investigated the ameliorating effects of p-hydroxybenzyl alcohol (HBA), an active phenolic ingredient of Gastrodia elata, on cycloheximide (CXM)-induced impairment of passive avoidance response and clarified the role of adrenal glands on the effect of HBA in rats. An adrenalectomy (ADX) caused the memory deficit from 1 to 3 days after surgery. Administration of corticosterone (CORT) plus glucose completely recovered the memory deficit caused by ADX, and this effect was better than that of glucose or CORT alone. HBA ameliorated the memory deficit induced by CXM in sham and ADX rats, but ADX partially blocked it. Furthermore, plasma glucose, epinephrine and adrenal steroid levels of ADX rats significantly decreased. Sham rats who received HBA had an increase in plasma glucose and adrenal steroid levels. Therefore, we suggest that the reversal of CXM-induced memory deficit by HBA was partially dependent on adrenal glands through the increase of the levels of plasma adrenal steroids.

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Section: Discussionsupporting

confidence: 90%

p-Hydroxybenzyl Alcohol, an Active Phenolic Ingredient of Gastrodia elata, Reverses the Cycloheximide-Induced Memory Deficit by Activating the Adrenal Gland in Rats

Chen

Tsai

et al. 2015

Am. J. Chin. Med.

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“…Even recent reviews of piracetam and related compounds state explicitly that, in spite of a tremendous amount of research in the latter 30 years, no commonly accepted mechanism of action has been established.£19, 151] Some benefit of piracetamlike nootropics in clinical studies of patients with mild to moderate degrees of dementia has been demonstrated, although the clinical response is estimated to lie in the 10 to 30% range.£152J The possible modes of action of nootropic drugs can be grouped in 4 categories: [152] • Effects on energy metabolism, such as increased adenylate kinase activity and increased glucose utilisation in hypoxic and anticholinergic conditions. • Effects on cholinergic mechanisms, such as increased high-affinity choline uptake and increased density of cortical muscarinic receptors.…”

Section: Nootropic Agentsmentioning

confidence: 99%

Cognition Enhancers in Age-Related Cognitive Decline

Riedel

Jolles

1996

Drugs & Aging

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A review of recently published studies on the effect of cognition enhancers in non-demented human study participants is presented. The heterogeneity of the therapeutic target, age-associated cognitive decline, can be improved by separately treating groups in whom age-extrinsic factors may underlie cognitive pathology. Standardisation of cognitive assessments is necessary, since many different tests are applied to answer the same question. Modelling cognitive dysfunction, either by pharmacological or nonpharmacological means, in humans is highly recommended since it allows hypotheses to be tested in a clearly operationalised way. Predictive validity of the currently applied models for the clinical situation remains a problem, however. The scopolamine (hyoscine) model has, to a reasonable extent, predictive validity for the cholinergic agents. The results of 67 single-dose studies and 30 multiple-dose studies are summarised. All single-dose studies and 14 multiple-dose studies were carried out in young or elderly human volunteers. In 45 of 81 volunteer studies, models of cognitive dysfunction were employed. The scopolamine model was the most used (n = 21); the other studies induced cognitive dysfunction by means of benzodiazepines (8), hypoxia (7), alcohol (5) and sleep-deprivation (4). The remaining 16 multiple-dose studies were clinical trials of a duration varying between 2 weeks and 1 year (average duration was 14 weeks). In these trials, the effects of cognition enhancers were assessed in elderly people in whom impairment of memory, psychomotor performance or cognitive function was determined. These included age-associated memory impairment (AAMI) and age-associated cognitive decline (AACD). There were many studies in which the cognition enhancing properties of substances in humans were reliably demonstrated. The cognition enhancing properties of substances that are widely used, such as caffeine, nicotine and vitamins, may already be active against AACD. New developments such as serotonin (5-hydroxytryptamine3; 5-HT3) antagonists and N-methyl-D-aspartate (NMDA) antagonists have provided marginal and disappointing results in AAMI. There is no cognition enhancer that has reliably and repeatedly been demonstrated to be efficacious for the treatment of AACD. However, this situation may change as the selectivity, specificity and adverse effect profiles of substances that are being developed for the treatment of AD may be expected to be improved in the future.

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“…[2] Some various drug groups that are approved by the US Food and Drug Administration are racetam, cholinergics, acetylcholinesterase inhibitors, AMPAkines, smart drugs, dopaminergics, nootropic vitamins, and neurohormones. [1] Although the mechanism of action of nootropics is still unknown, it is speculated that they improve cognition be being mildly cholinergic or anti-GABAergic.…”

Section: Introductionmentioning

confidence: 99%

“…[5] There is evidence that it can increase nitric National Journal of Physiology, Pharmacy and Pharmacology 432 2018 | Vol 8 | Issue 3 oxide (NO) activity in the cerebral cortex [6] and has shown to reverse memory defects in rats with cholinergic deficits, showing possible cholinergic effects. [2] Even though it's mode of action is not clear, [5] several potential mechanisms have been suggested, which includes high-affinity choline uptake [2] and increasing NO synthase (NOS) activity in the cerebral cortex in rats. [6] There has been an interest regarding pramiracetam and other piracetam derivatives in the treatment of disorders related to Alzheimer's disease, [7] cognition, epilepsy, seizures, neurodegenerative diseases, ischemia, and anxiety disorders.…”

Section: Introductionmentioning

confidence: 99%

“…[15] NO can be produced in several physiological processes by NOS that converts L-arginine to NO. [9] NO has been implicated to have a role in the myelination of the developing [2] brains as well as being associated with an increase in central nervous system myelination in rats. [16,17] However, NO has been shown to be capable of being toxic to oligodendrocytes and can induce the degeneration of axons that may lead to the process of demyelination.…”

Section: Introductionmentioning

confidence: 99%

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The effect of pramiracetam in the myelination of the hippocampus in the BALB/c mouse (Mus musculus)

Angeles¹,

Ples²,

Vitor³

2018

Natl J Physiol Pharm Pharmacol

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Background: Pramiracetam is being used, particularly by students, to increase cognitive function and enhance learning and memory. There are currently sparse data on the effect of pramiracetam, particularly in the brain. One recent study showed that there is an increased nitric oxide synthase (NOS) in systemically administered pramiracetam. Aims and Objectives: To determine if there would be a demyelinating effect in the hippocampus that is a sign of neurological damage due to increasing nitric oxide synthase. Materials and Methods: A total of fifteen mice were given 200 and 600 mg/kg dose of pramiracetam for qualitative histological comparison of their hippocampal myelination. After administration with food of the pramiracetam for 75 days, the mice were sacrificed and the brains were then extracted intact, and sagittal sections of the brain were made and stained with the Klüver-Barrera method. Hippocampi were analyzed using a compound microscope to observe for demyelination and neuronal degeneration. Results: Based on histological analysis, there were no signs of demyelination in the hippocampus of the Mus musculus brain. This may indicate that pramiracetam does not cause demyelination that may be due to increased NO production. Conclusion: Pramiracetam may be safe to take at doses of 200-600 mg/kg without any demyelinating effects in mouse.

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In search of the mechanism of action of the nootropics: New insights and potential clinical implications

Cited by 21 publications

References 51 publications

p-Hydroxybenzyl Alcohol, an Active Phenolic Ingredient of Gastrodia elata, Reverses the Cycloheximide-Induced Memory Deficit by Activating the Adrenal Gland in Rats

p-Hydroxybenzyl Alcohol, an Active Phenolic Ingredient of Gastrodia elata, Reverses the Cycloheximide-Induced Memory Deficit by Activating the Adrenal Gland in Rats

Cognition Enhancers in Age-Related Cognitive Decline

The effect of pramiracetam in the myelination of the hippocampus in the BALB/c mouse (Mus musculus)

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