Genetic contribution to the P3 in young and middle-aged adults

被引:17
作者
Smit, Dirk J. A.
Posthuma, Danielle
Boomsma, Dorret I.
de Geus, Eco J. C.
机构
[1] Vrije Univ Amsterdam, FPP, NL-1081 BT Amsterdam, Netherlands
[2] Vrije Univ Amsterdam, Dept Biol Psychol, Amsterdam, Netherlands
[3] Vrije Univ Amsterdam, Ctr Neurogenom & Cognit Res, Amsterdam, Netherlands
关键词
EVENT-RELATED POTENTIALS; BRAIN POTENTIALS; HUMAN ELECTROENCEPHALOGRAM; LINKAGE DISEQUILIBRIUM; ATTENTIONAL BLINK; ADOLESCENT TWINS; CLINICAL UTILITY; USE DISORDERS; ALCOHOLISM; AMPLITUDE;
D O I
10.1375/twin.10.2.335
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
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 (similar to 50%) and latency (similar to 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.
引用
收藏
页码:335 / 347
页数:13
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