Psychopathology of SCZ was rated by the positive and negative syndrome scale (PANSS), while cognitive function and P50 inhibition of subjects were assessed by the MATRICS Consensus Cognitive Battery (MCCB) and the electroencephalography system.
The CHRNA7 gene encoding the α7 nicotinic acetylcholine receptor (nAChR) has repeatedly been linked with schizophrenia and the P50 sensory gating deficit.
Following reports of SG improvements in low P50 suppressing SCZ patients and healthy participants with the α7 agonist, CDP-choline, this pilot study examined the combined modulatory effect of CDP-choline (500 mg) and galantamine (16 mg), a nAChR positive allosteric modulator and acetylcholinesterase inhibitor, on SG to speech stimuli in twenty-four SCZ patients in a randomized, double-blind and placebo-controlled design.
Our findings provide insight into the mechanisms of P50 suppression in schizophrenia and could potentially improve the performance of early identification and diagnosis of schizophrenia for the earliest intervention.
Associated with alpha 7 nicotinic acetylcholine receptor (α7 nAChR) dysfunction and shown to be improved with nicotine and α7 nAChR agonists, SG has recently been shown to be improved in low P50 suppressing SCZ patients following acute CDP-choline treatment.
PERG results showed a significant increase of the P50 implicit time in schizophrenia patients compared with controls (t(55) = 2.1, p < .05, d = 0.55) and a significant increase of the N95 implicit time in schizophrenia patients compared with controls (t(55) = 4.2; p < .001, d = 0.66).
We examined two candidate mechanisms of AVH in patients with BPD, suggested to underlie sensory processing systems that contribute to psychotic symptoms in patients with schizophrenia; sensory gating (P50 ratio and P50 difference) and change detection (mismatch negativity; MMN).
Some of the psychophysiological endophenotypes that have been studied for schizophrenia include prepulse inhibition of the startle response, the antisaccadic task assessing frontal lobe function, inhibition of the P50 event-related potential (ERP), and other auditory ERP measures.
These findings suggest that the P50 sensory gating deficits identified in Chinese patients with schizophrenia may not be involved in the psychopathology of the illness.
PPI and P50 gating measures demonstrate substantially increased heritability in schizophrenia families with a higher genetic vulnerability for illness, providing further support for the commonality of genes underlying both schizophrenia and gating measures.
Three electrophysiological endophenotypes are routinely studied in schizophrenia (SCZ): smooth pursuit eye movement (SPEM) dysfunction, deficits in P50 auditory-evoked potential inhibition, and saccadic inhibition deficits.
The present findings suggest that COMT Val(108/158)Met polymorphism may not contribute to the risk of schizophrenia and to the P50 deficits, but may contribute to the negative symptoms of schizophrenia among Han Chinese.
We examined the association of KMO polymorphisms with general neuropsychological performance and P50 gating in a sample of 150 schizophrenia and 95 healthy controls.
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.
No effect of polymorphisms in the non-duplicated region of the CHRNA7 gene on sensory gating P50 ratios in patients with schizophrenia and bipolar disorder.
A CHRNA7 genotype associated with schizophrenia was correlated with diminished P50 inhibition in the placebo-treated infants, but not in the choline-treated infants.
We investigated two neurophysiological endophenotypes of schizophrenia - P50 sensory gating and mismatch negativity in 22q11.2DS subject and evaluated their association with catechol O-methyltransferase (COMT) and proline dehydrogenase (PRODH) genetic variants.
We find that P50 and PPI may be influenced by COMT rs4680 polymorphisms in schizophrenia; more excitingly, we find that P50 might be influenced by COMT rs737865 polymorphisms and PPI may be influenced by COMT rs165599 polymorphisms in schizophrenia, and their mutations are associated with the reduction of the risk of P50 or PPI defects in schizophrenia.
P50 amplitude may, therefore, be a sensitive marker of nicotinic dysfunction in individuals with familial risk for schizophrenia, which is mediated through mechanisms (e.g., α₄β₂ receptors) that are distinct from those (e.g., α₇ receptors) that mediate P50 gating.
The P50 event-related potential sensory gating deficit, a failure to inhibit responses to repeated stimuli, is a leading endophenotype for schizophrenia (SZ).