The separate and combined effects of monoamine oxidase inhibition and nicotine on P50 sensory gating.

What Was Tested

The paper reports a study of Therapeutic nicotine (patch, non-peptide), published as a randomized controlled trial.

The cognitive effects of nicotine in humans remain a topic of great interest, due to the continued prevalence of cigarette smoking in society as well as the hypothesis that cognitively impaired populations such as schizophrenia patients use nicotine as a means of self-medicating against deficits of sensory gating.

However, chronic smoking can predispose individuals to robust monoamine oxidase (MAO) inhibition, and thus far, the effect of MAO inhibition on human sensory gating is unknown.

Who Took Part

The age groups tagged for this paper are adults, both men and women.

How the Study Was Run

The researchers set it up as a randomized, double-blind and crossover study.

Because people in this Therapeutic nicotine (patch, non-peptide) study were split into groups at random, differences between the groups are less likely to reflect who happened to join each one.

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

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

What Was Measured

Topics PubMed links to this paper include Evoked Potentials, Moclobemide, Monoamine Oxidase Inhibitors, Nicotine, Schizophrenia, Sensory Gating and Smoking.

What This Means in Plain Language

The paper is a randomized, double-blind and crossover study of Therapeutic nicotine (patch, non-peptide).

Its findings take up roughly 3 sentences of the abstract and are left out here on purpose; the source paper is the place to read them.

The publication is from 2015 (Psychopharmacology), a journal based in Germany.

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