Noopept

Authors:

Matěj Malík, Pavel Tlustoš

Findings:

This review provides an overview of nootropics ('smart drugs'), substances claimed to improve cognitive functions like thinking, learning, and memory, particularly when impaired. It categorizes nootropics (classical compounds, brain metabolism enhancers, cholinergics, plants/extracts), discusses their uses, mechanisms, dosages, side effects, and contraindications based on existing literature. While potentially beneficial for cognitive impairment, the review expresses concern and advises against use by healthy individuals due to insufficient evidence of efficacy and safety, especially long-term.

Participants:

This is a literature review covering studies involving various populations, including individuals with impaired cognitive functions (e.g., brain injury, dementia, Alzheimer's disease, minimal brain dysfunction, fatigue, exhaustion, schizophrenia, hyperkinetic disorder), healthy individuals (including students and healthy males), and animal models (rats, mice, male chicks).

Dosage:

Specific dosages mentioned include: Deanol (DMAE): 500–2000 mg daily; Meclofenoxate: 500–2000 mg daily; Nicergoline: 30–60 mg daily; Piracetam: 4–8 g/day infusion (acute), 2–4 g/day maintenance; Pyritinol: 300-600+ mg daily (divided); Vinpocetine: 10–30 mg daily; Naftidrofuryl: 300-600 mg/day (divided); Dihydroergotoxine: up to 6 mg daily; Phosphatidylcholine: 1200 mg 3x/day (prevention), 10-15+ g/day (patients); Ginseng: 200 mg standardized extract or 0.5-2 g dry root daily; Ginkgo: 120–300 mg standardized extract daily; Centella asiatica: 600 mg dried leaves or 60-120 mg standardized extract daily; Ashwagandha: 6-10 g root or 750-1250 mg extract daily; Bacopa monnieri: 5-12 mL liquid extract or 200-400 mg standardized extract daily (adults); Guarana: 75 mg extract tablet; Eleuthero: 2-3 g dried root or 20-40 drops liquid extract daily; Rhodiola: 100-170 mg extract daily (long-term) or 360-600 mg (1% rosavin) daily; Schisandra: 2-6 g dried fruit daily; Maca: 1.5–3 g root powder daily.

Study Quality Assessment:

The text identifies itself as a literature review including original research articles, meta-analyses, systematic reviews, and relevant animal studies. It mentions specific study designs from the reviewed literature (e.g., 'double-blind study', 'placebo-controlled', 'randomized in vivo studies', 'EEG analysis', 'EEG/ERP mapping study'). Limitations acknowledged include 'few studies on healthy young individuals' and 'lack of clinical evidence regarding their efficacy, safety, and social consequences, especially in long-term use' by healthy individuals. The funding source for the publication is mentioned.

All Effects:

Authors:

Pelsman A. et. Al.

Findings:

GVS-111 demonstrated dose-dependent neuroprotection against H(2)O(2)-induced oxidative stress in normal human cortical neurons, increasing survival by inhibiting free radicals and lipid peroxidation (antioxidant mechanism). It showed higher neuroprotection than Piracetam and other tested antioxidants. Chronic GVS-111 treatment also reduced degenerative changes and enhanced survival in Down's syndrome cortical neurons.

Participants:

In vitro models using normal human cortical neurons and Down's syndrome (DS) human cortical neurons. MeSH terms suggest neurons derived from aborted fetuses.

Dosage:

Dose-dependent neuroprotective activity from 10nM to 100 microM, with an IC(50) value of 1.21+/-0.07 microM against H(2)O(2) damage in normal neurons. Chronic treatment mentioned for DS neurons, but specific dose/duration not detailed.

Study Quality Assessment:

Comparative Study. Methods involved treating normal neurons with H(2)O(2) or FeSO(4) and DS neurons with chronic GVS-111. Measured morphological changes, neuronal survival, intracellular free radicals, and lipid peroxidation. Compared GVS-111 effects to Piracetam, Vitamin E, propyl gallate, and N-tert-butyl-2-sulpho-phenylnitrone (s-PBN). Funding mentioned: Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Grant HD38466/HD/NICHD NIH HHS/United States.

All Effects:

Findings:

Noopept pretreatment (10 μM for 72h) protected PC12 cells against Aβ25-35 (5 μM for 24h)-induced injury. It improved cell viability, reduced apoptosis, decreased intracellular reactive oxygen species (ROS) and calcium levels, enhanced mitochondrial membrane potential, attenuated tau hyperphosphorylation at Ser396, and ameliorated alterations in neurite outgrowth. The study concludes Noopept protects cells by inhibiting oxidative damage, calcium overload, suppressing the mitochondrial apoptotic pathway, decreasing tau phosphorylation, and restoring cell morphology.

Participants:

AD-related cellular model: PC12 cells.

Dosage:

10 μM Noopept added to cell medium 72 hours before exposure to 5 μM Аβ 25-35 for 24 h.

Study Quality Assessment:

Cellular study using PC12 cells. Methods mentioned include evaluation of cell viability (MTT assay), apoptosis (Annexin-V-FITC/propidium iodide staining), calcium homeostasis, ROS level, mitochondrial function, tau phosphorylation (Western blot for Ser396), and neurite outgrowth (IIIβ-tubulin immunopositivity). Experimental replication is mentioned (e.g., 'Three independent experiments were carried out in triplicate'). Publication type listed as 'Research Support, Non-U.S. Gov't'.

All Effects:

Participants:

Animal model: NMRI mice following olfactory bulbectomy

Study Quality Assessment:

Animal model used: NMRI mice following olfactory bulbectomy, modeling Alzheimer's disease (AD)-like characteristics.