Genetic Contribution to the P3 in Young and Middle-Aged Adults

Abstract

Previous studies in young and adolescent twins suggested substantial genetic contributions to the amplitude and latency of the P3 evoked by targets in an oddball paradigm. Here we examined whether these findings can be generalized to adult samples. A total of 651 twins and siblings from 292 families participated in a visual oddball task. In half of the subjects the age centered around 26 (young adult cohort), in the other half the age centered around 49 (middle-aged adult cohort). P3 peak amplitude and latency were scored for 3 midline leads Pz, Cz, and Fz. No cohort differences in heritability were found. P3 amplitude (∼50%) and latency (∼45%) were moderately heritable for the 3 leads. A single genetic factor influenced latency at all electrodes, suggesting a single P3 timing mechanism. Specific genetic factors influenced amplitude at each lead, suggesting local modulation of the P3 once triggered. Genetic analysis of the full event-related potential waveform showed that P3 heritability barely changes from about 100 ms before to 100 ms after the peak. Age differences are restricted to differences in means and variances, but the proportion of genetic variance as part of the total variance of midline P3 amplitude and latency does not change from young to middle-aged adulthood.

P3a Amplitude Predicts Successful Treatment Program Completion in Substance-Dependent Individuals

“…P3 amplitudes are reliably modified by a variety of task conditions, such as stimulus rarity and task difficulty, which have led to the increasing use of P3 amplitude as a measure of processing capacity or a relative index of the allocation of attentional resources to a task (Kok, 2001). Additionally, P3 amplitude has been shown to be a genetically heritable trait (Katsanis, Iacono, McGue, & Carlson, 1997;Smit, Posthuma, Boomsma, & de Geus, 2007), making it an attractive candidate as an endophenotype for genetically influenced psychopathology. 670 N.…”

The Adult Netherlands Twin Register: Twenty-Five Years of Survey and Biological Data Collection

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“…More recent studies have provided further evidence for genetic influences on P3 and addressed a number of related questions, including genetic covariation between P3 latency measured in a delayed response working memory task and working memory performance (Hansell et al, 2005), genetic specificity of P3 as evidenced by the lack of genetic overlap with other ERP measures such as MMN or P50 (Hall et al, 2006a), invariance of P3 heritability across the lifespan demonstrated using cross-sectional comparison of young and middle-aged adult cohorts (Smit et al, 2007a), genetic influences on age-related decrease of P3 amplitude using longitudinal analysis spanning ages from 17 to 23 (Carlson and Iacono, 2006) and genetic influences on neural oscillations contributing to P3 assessed using time-frequency decomposition of event-related EEG (Ethridge et al, 2012). …”