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Modulating Cognition Using Transcranial Direct Current Stimulation of the Cerebellum

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Tolcapone improves cognition and cortical information processing in normal human subjects.

José A Apud¹, Venkata Mattay, Jingshan Chen

¹Genes, Cognition and Psychosis Program, Clinical Brain Disorders Branch, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20854, USA.

Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology

|October 26, 2006

Summary

Tolcapone, a COMT inhibitor, enhanced executive functions and working memory in healthy adults. This non-stimulant drug shows promise for treating prefrontal cortex executive dysfunction, particularly in specific genetic profiles.

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Area of Science:

Neuroscience
Pharmacology
Genetics

Background:

Prefrontal cortical dopamine (DA) is crucial for executive functions like attention and working memory.
Existing stimulant drugs for cognitive enhancement have limitations.
A COMT gene polymorphism influences prefrontal cognition, suggesting a novel therapeutic target.

Purpose of the Study:

To investigate the effects of tolcapone, a COMT inhibitor, on prefrontal cognitive functions.
To explore tolcapone's efficacy as a non-stimulant approach for executive dysfunction.
To examine drug effects stratified by COMT (val158met) genotype.

Main Methods:

Randomized, double-blind, placebo-controlled, crossover study design.
Inclusion of 47 healthy volunteers stratified by COMT (val158met) genotype.
Neuropsychological testing and fMRI for assessing prefrontal information processing.

Main Results:

Tolcapone significantly improved executive function and verbal episodic memory.
A significant drug-by-genotype interaction was observed for memory, with val/val genotypes improving and met/met genotypes worsening.
fMRI showed enhanced prefrontal cortex information processing efficiency during working memory tasks with tolcapone.

Conclusions:

Tolcapone enhances prefrontal cortical function in humans via COMT inhibition.
This non-stimulant drug offers a potential new strategy for cognitive enhancement.
Results align with animal and computational models of enhanced DA signaling in the prefrontal cortex.