Genetic overlap between P300, P50, and duration mismatch negativity

Hall, Matt G.; Schulze, Katja; Bramon, Elvira; Murray, Robin M.; Sham, Pak C.; Rijsdijk, Frühling

doi:10.1002/ajmg.b.30318

Cited by 40 publications

(33 citation statements)

References 45 publications

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“…The high similarity of maximum MMN amplitude in MZ twins is consistent with previous ERP studies [8,36]. These results suggest genetic contributions to the MMNm.…”

Section: Discussionsupporting

confidence: 91%

Familial Influences on Mismatch Negativity and Its Association with Plasma Glutamate Level: A Magnetoencephalographic Study in Twins

et al. 2016

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Mismatch negativity (MMN) or its magnetic counterpart (magnetic mismatch negativity; MMNm) is regarded as a promising biomarker for schizophrenia. Previous electroencephalographic studies of MMN have demonstrated a moderate-to-high heritability for MMN amplitudes. N-methyl-D-aspartate receptor-dependent glutamatergic neurotransmission is implicated in MMN generation. We hypothesized that the differences between identical twins in MMNm variables might be associated with differences in plasma levels of amino acids involved in glutamatergic neurotransmission. Thirty-three pairs of monozygotic (MZ) and 10 pairs of dizygotic (DZ) twins underwent MMNm recording. The MMNm in response to tone duration changes, tone frequency changes, and phonemic changes was recorded using 204-channel magnetoencephalography. Of these, 26 MZ and 7 DZ twin pairs underwent blood sampling for determination of plasma amino acid levels. MMNm peak strength showed relatively high correlations in both MZ and DZ twin pairs. The differences in MMNm latencies tended to correlate with the differences in plasma amino acid levels within MZ pairs, while no significant correlation was observed after the Bonferroni correction. We observed a familial trait in MMNm strength. The differences in MMN latency in MZ twins might be influenced by changes in glutamate levels and glutamate-glutamine cycling; however, the results need to be replicated.

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“…The high similarity of maximum MMN amplitude in MZ twins is consistent with previous ERP studies [8,36]. These results suggest genetic contributions to the MMNm.…”

Section: Discussionsupporting

confidence: 91%

Familial Influences on Mismatch Negativity and Its Association with Plasma Glutamate Level: A Magnetoencephalographic Study in Twins

et al. 2016

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“…Impaired P50 sensory-gating responses, reduced amplitude in auditory N100, P200, and P300 ERP, and delayed latency in P300 ERP are robust findings in patients with SCZ and BPD and in their unaffected biological relatives [Bramon et al, 2004; Hall et al, 2006b, 2009; Turetsky et al, 2007; Salisbury et al, 2010] and have been suggested as likely endophenotypes [Braff et al, 2007a]. These ERPs components appear to be uncorrelated with one another, suggesting each may be mediated by distinct mechanisms [Hall et al, 2006a]. The underlying mechanisms and brain circuits subserving each ERP activity have been extensively studied using drug challenge investigations and animal models [Turetsky et al, 2007; Braff et al, 2007a; Javitt et al, 2008].…”

Section: Introductionmentioning

confidence: 99%

Neurophysiologic effect of GWAS derived schizophrenia and bipolar risk variants

Hall

Levy

Salisbury

et al. 2013

American J of Med Genetics Pt B

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Genome-wide association studies (GWAS) have identified multiple single nucleotide polymorphisms (SNPs) as disease associated variants for schizophrenia (SCZ), bipolar disorder (BPD), or both. Although these results are statistically robust, the functional effects of these variants and their role in the pathophysiology of SCZ or BPD remain unclear. Dissecting the effects of risk genes on distinct domains of brain function can provide important biological insights into the mechanisms by which these genes may confer illness risk. This study used quantitative event related potentials to characterize the neurophysiological effects of well-documented GWAS-derived SCZ/BPD susceptibility variants in order to map gene effects onto important domains of brain function. We genotyped 199 patients with DSM-IV diagnoses of SCZ or BPD and 74 healthy control subjects for 19 risk SNPs derived from previous GWAS findings and tested their association with five neurophysiologic traits (P3 amplitude, P3 latency, N1 amplitude, P2 amplitude, and P50 sensory gating responses) known to be abnormal in psychosis. The TCF4 SNP rs17512836 risk allele showed a significant association with reduced auditory P3 amplitude (P =0.00016) after correction for multiple testing. The same allele was also associated with delayed P3 latency (P =0.005). Our results suggest that a SCZ risk variant in TCF4 is associated with neurophysiologic traits thought to index attention and working memory abnormalities in psychotic disorders. These findings suggest a mechanism by which TCF4 may contribute to the neurobiological basis of psychotic illness.

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“…Although these findings are often contradictory in terms of the co-occurrence of auditory ERP abnormalities in the same patient population, discrepancies might be attributed to the fact that the above-described ERPs are influenced by different factors such as stimulus parameters, attention, arousal, smoking status, or psychotropic medication [25][26][27].…”

Section: Discussionmentioning

confidence: 98%