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BACKGROUND: Reinforcement learning (RL) impairment has been observed in chronic schizophrenia and first-episode psychosis. Yet, there is a paucity of research of RL impairment in individuals at clinical high-risk (CHR) for psychosis. The current study aimed to examine RL performance in a representative cohort of Chinese CHR subjects, with particular focus on its relationship with primary negative symptoms (PNS). METHODS: Ninety-seven Chinese individuals with CHR for psychosis, aged 15–40 years, were recruited from a territory-wide specialized early intervention service for psychosis in Hong Kong. CHR status was verified using Comprehensive Assessment of At-Risk Mental State (CAARMS). Thirty-four demographically-matched healthy controls were recruited as a comparison group. Each subject completed two computerized RL tasks (Go-No-Go, GNG and Gains-Loss Avoidance GLA tasks) which have been studied in chronic and first-episode schizophrenia patients. In both tasks, rapid / gradual and positive / negative RL measures were derived for analyses. CHR subjects were categorized as having PNS if they had (1) global score ≥ 3 on at least two of the following SANS subscales: Affective flattening, Alogia, Avolition-apathy or Anhednoia-asociality; and (2) no or clinically non-significant depression with total score < 16 in Montgomery-Asberg Depression Rating Scale (MADRS). RESULTS: On GNG task, three-group comparison (PNS, non-PNS, control groups) revealed significant difference in RL accuracy, with post-hoc contrasts showing that controls performed better than both PNS and non-PNS groups in gradual positive RL. No between-group difference in Go-response bias or rapid learning was observed. On GLA task, main effect of group was noted in three-group comparison analysis on RL accuracy. Post-hoc tests indicated that PNS group displayed significantly lower accuracy than both non-PNS group and controls in gradual positive and negative RL. Additionally, PNS group exhibited significantly lower overall and block-1 win-stay rates than controls. DISCUSSION: Our results indicate RL impairment in CHR sample. In particular, such RL impairment was more evident in CHR subjects presenting with PNS relative to those without PNS. Further investigation is required to verify and confirm our findings on the relationship between negative symptoms and RL deficits. In addition, a prospective follow-up of our CHR cohort will help clarify the potential utility of baseline RL impairment in enhancing prediction of psychosis transition at follow-up.

Background Subjective quality of life (SQoL) is an important outcome domain in individuals with at-risk mental state (ARMS) for psychosis. In an effort to better understand and maximize SQoL in ARMS populations, an increasing number of research has been conducted to investigate factors determining SQoL. This study aimed to examine clinical, functional and cognitive correlates of SQoL in Chinese young people presenting with ARMS in Hong Kong. Methods This is a naturalistic prospective study examining the longitudinal course of ARMS and prediction of psychosis in Hong Kong. In total, 110 Chinese participants aged 15 to 40 years presenting with ARMS were recruited from a territory-wide specialized early intervention service for psychosis. ARMS status was verified using Comprehensive Assessment for At-Risk Mental State (CAARMS). Assessments encompassing symptom profiles (Positive and Negative Syndrome Scale, PANSS; Montgomery-Asberg Depression Rating Scale, MADRS; Brief Negative Symptom Scale, BNSS), functioning (Social and Occupational Functioning Rating Scale, SOFAS) and a brief battery of cognitive tests was conducted. A validated Chinese version of SF12 questionnaire was used to measure SQoL. The current analysis focused on data collected at baseline. Results Of 110 ARMS participants, 48.2% were male. The mean age and educational level of the sample was 20.9 years (S.D.=6.7) and 11.4 years (S.D.=2.6), respectively. Correlation analyses revealed that SF12 mental health score was correlated with MADRS total score, BNSS total score and SOFAS score, while SF12 physical health score was correlated with PANSS positive symptom score only (p

Background: While it is well established that schizophrenia is highly heritable, the genetic architecture of the disorder remains unclear. Reinforcement learning deficits, which have been consistently shown to be present in schizophrenia patients, may represent a potential endophenotypic marker for the disorder. This study aims to compare early schizophrenia patients and their nonpsychotic siblings in reinforcement learning performance.

Background Neurocognitive impairment is a core feature of schizophrenia, and has been observed among healthy non-psychotic siblings of schizophrenia patients as well as individuals at clinical high-risk (CHR) for psychosis. Thus far, few studies have directly contrasted neurocognitive performance between non-psychotic siblings and CHR samples. Potential differential patterns of neurocognitive deficits among schizophrenia patients, familial high-risk and CHR samples remain to be clarified. This study aimed to compare neurocognitive functions among first-episode schizophrenia (FES) patients, their non-psychotic siblings, CHR individuals, and healthy controls. Methods FES patients (n=69, mean age=25.3) and CHR individuals (n=97, mean age=21.1) without family history of psychosis were recruited from a territory-wide specialized early intervention service for psychosis in Hong Kong. A group of non-psychotic siblings of FES patients (n=50, mean age=25.4) and healthy controls (HC) (n=68, mean age=24.5) were also recruited. A standardized battery of neurocognitive tests encompassing working memory, processing speed, executive function, visual memory, verbal learning, and sustained attention was administered. Group differences were examined using analysis of covariance (ACOVA) with Bonferroni correction applied for statistical significance (P

The expansion of a hexanucleotide (GGGGCC) repeat in C9ORF72 is the most common cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Both the function of C9ORF72 and the mechanism by which the repeat expansion drives neuropathology are unknown. To examine whether C9ORF72 haploinsufficiency induces neurological disease, we created a C9orf72-deficient mouse line. Null mice developed a robust immune phenotype characterized by myeloid expansion, T cell activation and increased plasma cells. Mice also presented with elevated autoantibodies and evidence of immune-mediated glomerulonephropathy. Collectively, our data suggest that C9orf72 regulates immune homeostasis and an autoimmune response reminiscent of systemic lupus erythematosus (SLE) occurs in its absence. We further imply that haploinsufficiency is unlikely to be the causative factor in C9ALS/FTD pathology.