Schizophrenia, a complex psychiatric disorder, clinically encompasses heterogeneous syndromal presentations and pathogenetically involves complicated neurobiological process. The lack of specific corresponding relationships between various phenotypes and neurobiological bases makes it difficult to elucidate the etiology of this mental illness, which is particularly true based upon the phenomenological approach of the contemporary psychiatric classification system. To address this issue, utilizing the concept of endophenotype, i.e. a state-independent intermediate marker, in schizophrenia research has been proposed and widely adopted 
. A growing body of evidence has suggested several candidate endophenotypes in schizophrenia, including neurophysiological markers (e.g. auditory event-related potentials (ERPs), such as P50, P300 and Mismatch Negativity), and neuropsychological tests (e.g. attention, memory, working memory, and executive function), some of which have been successfully linked to specific genetic components 
. Therefore, studying endophenotypes in schizophrenia may lead to a better understanding of this complex illness.
Of neurophysiological markers, P50 sensory gating is regarded to be a candidate endophenotype for schizophrenia 
. P50, indicating a preattentional electroencephalographic activity, is a positive wave emerging around 50 msec after an auditory stimulus. In a healthy person, the amplitude of P50 wave corresponding to the second click (S2) is significantly smaller than that corresponding to the first (S1). P50 gating ratio, derived from the S2 amplitude divided by S1 amplitude, is the most commonly used index for P50 sensory gating. P50 sensory gating refers to the phenomenon that the central nervous system modulates its sensitivity to incoming stimuli 
. Regardless of disease state, P50 sensory gating deficit exists in both patients with full-blown schizophrenia and their unaffected relatives with effect sizes of 0.92–1.29 and 0.79, respectively 
. For schizophrenia patients, there is little evidence for any association between certain symptomatology and P50 gating ratio 
. Furthermore, P50 sensory gating has been successfully linked to CHRNA7, the gene for alpha-7 subunit of nicotinic receptor, located on chromosome 15q13–14 
. Indeed, cigarette smoking has been proved to be able to transiently normalize impaired P50 gating ratio in schizophrenia patients 
. It has been related to the high prevalence of cigarette smoking in schizophrenia patients, by which, as self-medication, psychiatric symptoms can be alleviated through improving P50 sensory gating deficits 
. Nevertheless, it remains unclear about the relationship between P50 sensory gating and long-term nicotine exposure. Taken together, these findings support that P50 sensory gating may be qualified as an endophenotype for schizophrenia.
Abundant evidence exists that schizophrenia patients have a poorer performance of neurocognitive function across individual domains (e.g. sustained attention, memory, executive function, working memory, and spatial ability) and global indices (e.g. Performance IQ, Verbal IQ, and Full IQ), some of which have been proposed to be candidate endophenotypes for schizophrenia 
. However, it is an issue of grave importance choosing appropriate tools to measure specific neurocognitive performances. Continuous Performance Test (CPT) and Wisconsin Card Sorting Test (WCST) have been widely employed to study neuropsychological deficits in schizophrenia; the former is used to assess sustained attention and the latter executive function. Impaired CPT performance can be found in both schizophrenia patients (effect size: 0.45–3.30) and unaffected relatives (effect size: 0.46–2.97) compared to healthy subjects 
. Likewise, the effect sizes for WCST in schizophrenia patients and unaffected relatives have been reported to be 0.8–1.0 and 0.26, respectively 
. Accordingly, both CPT and WCST may be candidate measures of neuropsychological endophenotypes for schizophrenia.
Endophenotypes in schizophrenia, in addition to facilitating research in pathogenesis, may serve another purpose of crucial significance – to refine the classification system, i.e. a clinical purpose 
. However, the clinical utility of any single candidate endophenotype for schizophrenia to date is limited in contrast to a rapidly growing body of evidence from etiological studies using endophenotypes. This may be because the impairment in either neurophysiological or neuropsychological markers does not exclusively exist in schizophrenia. Taking P50 for example, P50 gating deficits can be observed in bipolar disorder, Huntington’s disease, Alzheimer’s dementia, obsessive-compulsive disorder and attention-deficit/hyperactivity disorder (ADHD) 
. Similarly, both CPT and WCST impairments also occur in many psychiatric disorders, such as bipolar disorder, mild cognitive impairment, Alzheimer’s dementia, ADHD and autistic disorder 
. One approach to address this issue is to build a diagnostic model by incorporating different markers. Theoretically, the more diversity the markers represent, the more power the model would have in discriminating patients and healthy subjects 
. Of note, one recent study depicted there existed no associations between P50 gating and neurocognitive domains, including sustained attention, executive function, working memory, verbal learning and memory, visual memory and proceed speed 
.To the present, there have only been few studies focusing on developing models to differentiate schizophrenia from healthy controls or other mental disorders by a combination of different neurophysiological markers, neuropsychological indices, or both 
In the present study, we aimed to construct a diagnostic model for schizophrenia by incorporating P50 sensory gating in combination with other neuropsychological batteries. This work may contribute to the existing literature on P50 sensory gating in subjects of Chinese ethnicity.