There is increasing awareness that oxidative stress may be implicated in the pathophysiology of autism spectrum disorder (ASD). Here we aimed to investigate blood oxidative stress marker profile in ASD children by a meta-analysis. Two independent investigators systematically searched Web of Science, PubMed, and Cochrane Library and extracted data from 87 studies with 4928 ASD children and 4181 healthy control (HC) children. The meta-analysis showed that blood concentrations of oxidative glutathione (GSSG), malondialdehyde, homocysteine, S-adenosylhomocysteine, nitric oxide, and copper were higher in children with ASD than that of HC children. In contrast, blood reduced glutathione (GSH), total glutathione (tGSH), GSH/GSSG, tGSH/GSSG, methionine, cysteine, vitamin B9, vitamin D, vitamin B12, vitamin E, S-adenosylmethionine/S-adenosylhomocysteine, and calcium concentrations were significantly reduced in children with ASD relative to HC children. However, there were no significance differences between ASD children and HC children for the other 17 potential markers. Heterogeneities among studies were found for most markers, and meta-regressions indicated that age and publication year may influence the meta-analysis results. These results therefore clarified blood oxidative stress profile in children with ASD, strengthening clinical evidence of increased oxidative stress implicating in pathogenesis of ASD. Additionally, given the consistent and large effective size, glutathione metabolism biomarkers have the potential to inform early diagnosis of ASD.

The incidence of dementia based on DSM‐III criteria and the impact of age and education on the development of dementia using the data of a longitudinal community population survey is discussed. Study subjects were randomly sampled from the community and were assessed by a two‐stage procedure twice during a 5‐year period. The screening instrument was the Mini‐Mental State Examination and the second stage measures include a medical history and physical examination, a neurological examination and an intensive neuropsychiatric interview and testings (i.e. Blessed Dementia Scale, Activity of Daily Living, Fuld Object Memory Test and Block Design Test. All identified cases from the second stage interview were further verified by computed tomographic scan and laboratory tests. A total of 1970 subjects of non‐dementia aged 65 or older in 1987 were re‐surveyed after 5 years, of whom 114 new cases of dementia were identified. The incidence of dementia in total was 1.15% annually, 0.98% for males and 1.27% for females. The incidence for Alzheimer's disease, vascular dementia and dementia by other causes was 0.74, 0.33 and 0.08%, respectively. The highest rate (2.02%) was found in illiterate individuals. The incidence of dementia in the Shanghai cohort is similar to that from other countries. Age and education are closely related to the occurrence of dementia. While age increases by each 5 years for those aged 65 and over the likelihood of developing dementia increases nearly one‐fold (74%). Education shows great protective effect on the development of dementia. The non‐educated has a higher risk of suffering from dementia than does the educated.

Increasing evidence suggests that abnormal regulation of neurotrophic factors is involved in the etiology and pathogenesis of Autism Spectrum Disorder (ASD). However, clinical data on neurotrophic factor levels in children with ASD were inconsistent. Therefore, we performed a systematic review of peripheral blood neurotrophic factors levels in children with ASD, and quantitatively summarized the clinical data of peripheral blood neurotrophic factors in ASD children and healthy controls. A systematic search of PubMed and Web of Science identified 31 studies with 2627 ASD children and 4418 healthy controls to be included in the meta-analysis. The results of random effect meta-analysis showed that the peripheral blood levels of brain-derived neurotrophic factor (Hedges’ g = 0.302; 95% CI = 0.014 to 0.591; P = 0.040) , nerve growth factor (Hedges’ g = 0.395; 95% CI = 0.104 to 0.686; P = 0.008) and vascular endothelial growth factor (VEGF) (Hedges’ g = 0.097; 95% CI = 0.018 to 0.175; P = 0.016) in children with ASD were significantly higher than that of healthy controls, whereas blood neurotrophin-3 (Hedges’ g =  − 0.795; 95% CI =  − 1.723 to 0.134; P = 0.093) and neurotrophin-4 (Hedges’ g = 0.182; 95% CI =  − 0.285 to 0.650; P = 0.445) levels did not show significant differences between cases and controls. Taken together, these results clarified circulating neurotrophic factor profile in children with ASD, strengthening clinical evidence of neurotrophic factor aberrations in children with ASD.

Background Obesity is a serious worldwide public health problem, especially for people with mental disorders. Aim To explore the related factors of obesity by analyzing the metabolic indexes of patients with common mental disorders in stable stage. Methods Five hundred seventy-six subjects with major depressive disorder (MDD), bipolar disorder (BD) or schizophrenia (SCZ) were included, who received fixed drug dose and routine drug treatment for 2 years or more. Their venous blood was collected, and the blood metabolic indexes were analyzed. Results BD and SCZ are more prone to obesity than MDD. Multiple linear regression analysis showed that the value of BMI increased with the increase of age(B = 0.084, p < 0.001), TG(B = 0.355, p = 0.024), LDL(B = 0.697, p < 0.001), LDH(B = 0.011, p = 0.002), SCr(B = 0.051, p < 0.001), UA(B = 0.014, p < 0.001), HbA1c(B = 0.702, p = 0.004) and hsCRP(B = 0.101, p < 0.001). And It decreased with the increase of HDL(B = -1.493, p < 0.001). Discussion People with mental disorders should regularly check blood indicators and strengthen weight management to reduce the risk of obesity and promote their health.

Huntington’s disease (HD) is a hereditary autosomal dominant neurodegenerative disease. Although studies have shown that blood oxidative stress markers are dysregulated in HD patients, clinical data on the blood oxidative stress markers of HD patients is inconsistent. To better understand the pathogenesis of HD, we performed a systematic review and meta-analysis of blood oxidative stress markers in HD patients and healthy control (HC) subjects. A database search from PubMed and Web of Science identified 12 studies with 375 HD patients and 447 HC subjects in this meta-analysis. A random-effects meta-analysis showed that blood lipid peroxidation products (Hedges’ g=0.883, 95%CI=0.637 to 1.130, p<0.001), 8-hydroxyguanosine (Hedges’ g=1.727, 95%CI=0.489 to 2.965, p=0.006) levels, and the activity of glutathione peroxidase (Hedges’ g=2.026, 95%CI=0.570 to 3.482, p=0.006) were significantly increased in HD patients compared to controls. In contrast, reduced glutathione levels were lower in HD patients than in controls (Hedges’ g=−0.611, 95%CI=−1.016 to−0.207, p=0.003). However, blood superoxide dismutase, cholesterol, high-density lipoproteins, low-density lipoproteins, and triglycerides did not show significant differences between cases and controls. Taken together, this study clarified the associations between blood oxidative stress markers and HD, supporting the clinical evidence that HD is accompanied by increased oxidative stress.