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Nicotine fails to attenuate ketamine-induced cognitive deficits and negative and positive symptoms in humans: implications for schizophrenia.

Plain-language guide to PMID 22717030 (2012): double-blind randomized controlled trial of Therapeutic nicotine (patch, non-peptide) in 37 subjects.

Key Facts

PMID
22717030
Journal
Biological psychiatry
Year
2012
Study type
Randomized Controlled Trial
Authors
D'Souza DC et al. (10 authors)
DOI
10.1016/j.biopsych.2012.05.009
Registered trial
NCT00690170

What This Study Did, in Plain Language

What Was Tested

This randomized controlled trial looks at Therapeutic nicotine (patch, non-peptide).

The uncompetitive N-methyl-D-aspartate receptor (NMDAR) antagonist, ketamine, induces a range of symptoms resembling those seen in schizophrenia.

Enhancement of nicotinic acetylcholine receptor (nAChR) function may have potential as a treatment for the cognitive deficits and negative symptoms of schizophrenia.

Who Took Part

The abstract describes 37 subjects taking part.

PubMed indexes the participants as teenagers, adults and middle-aged adults.

The interactive effects of ketamine and nicotine were evaluated in 37 healthy subjects in a randomized, placebo-controlled, double-blind, crossover counterbalanced, 2 (intravenous ketamine or placebo) × 2 (intravenous nicotine or placebo) design.

How the Study Was Run

In design terms this was a randomized, double-blind, placebo-controlled and crossover study.

Random assignment meant chance, not the researchers, decided who got Therapeutic nicotine (patch, non-peptide) and who got the comparison, which limits bias.

Neither the subjects nor the staff measuring them knew who was on Therapeutic nicotine (patch, non-peptide), so expectations could not easily colour the readings.

The comparison arm used a placebo, so changes seen with Therapeutic nicotine (patch, non-peptide) could be set against what happens without it.

Each person switched between Therapeutic nicotine (patch, non-peptide) and the comparison at some point, usually with a gap in between.

Verbal and visual memory, sustained attention, working memory, response inhibition, emotion recognition, executive function, reaction time, motor function, and speed of processing were assessed once per test day, while negative and positive symptoms, perceptual alterations, and a number of feeling states were measured several times before and after administration of drugs.

What Was Measured

Topics PubMed links to this paper include Attention, Cognition, Cognition Disorders, Drug Interactions, Executive Function, Inhibition, Psychological and Ketamine.

What This Means in Plain Language

The paper is a randomized, double-blind and placebo-controlled study of Therapeutic nicotine (patch, non-peptide) in 37 subjects.

With fewer than 40 people, it is a small study, so it is better read as an early signal for further research than as a settled answer.

Its findings take up roughly 6 sentences of the abstract and are left out here on purpose; the source paper is the place to read them.

The publication is from 2012 (Biological psychiatry), a journal based in United States.

More context: the Therapeutic nicotine (patch, non-peptide) compound page, all human trials.

Our Notes on the Compound

Therapeutic nicotine (patch, non-peptide): Pure nicotine as a signaling tool, separated from smoking and vaping.

Related Pages

Source: PubMed record. This explanation is written by PeptideWhiz from the public record. For research and education only. Not medical advice; no dosing information is given.