Related Experiment Video
Updated: May 1, 2026

Orienteering as a Tool for Cognitive Research: An Implementation Guide
Published on: November 29, 2024
Effects and mechanisms of ginseng and ginsenosides on cognition
Imogen Smith1, Elizabeth M Williamson, Sophie Putnam
1School of Chemistry, Food and Nutritional Sciences and Pharmacy, University of Reading, Reading, Berkshire, UK.
Abstract:
Reviewed here is the existing evidence for the effects of ginseng extracts and isolated ginsenosides relevant to cognition in humans. Clinical studies in healthy volunteers and in patients with neurological disease or deficit, evidence from preclinical models of cognition, and pharmacokinetic data are considered. Conditions under which disease modification may indirectly benefit cognition but may not translate to cognitive benefits in healthy subjects are discussed. The number of chronic studies of ginseng effects in healthy individuals is limited, and the results from acute studies are inconsistent, making overall assessment of ginseng's efficacy as a cognitive enhancer premature. However, mechanistic results are encouraging; in particular, the ginsenosides Rg3 , Rh1 , Rh2 , Rb1 , Rd, Rg2 , and Rb3 , along with the aglycones protopanaxadiol and protopanaxatriol, warrant further attention. Compound K has a promising pharmacokinetic profile and can affect neurotransmission and neuroprotection. Properly conducted trials using standardized tests in healthy individuals reflecting the target population for ginseng supplementation are required to address inconsistencies in results from acute studies. The evidence summarized here suggests ginseng has potential, but unproven, benefits on cognition.
Related Concept Videos
Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists
Pharmacodynamics in Geriatric Patients: Effects of Age
Ligand-Gated Ion Channel Receptor: Gating Mechanism
Adrenergic Agonists: Indirect-Acting Agents
One mechanism involves depleting stored catecholamines by displacing them from synaptic vesicles. These agents, known as "displacers," are transported into vesicles at the expense of noradrenaline. Examples include amphetamine and tyramine, which lack a catechol moiety, resulting in prolonged action, improved oral...
CNS Stimulants: Cocaine, Amphetamines and Cannabinoids
Drugs Affecting Neurotransmitter Release or Uptake
