Anxiety and Depression in Adults with Autism Spectrum Disorder: A Systematic Review and Meta-analysis

Adults with autism spectrum disorder (ASD) are thought to be at disproportionate risk of developing mental health comorbidities, with anxiety and depression being considered most prominent amongst these. Yet, no systematic review has been carried out to date to examine rates of both anxiety and depression focusing specifically on adults with ASD. This systematic review and meta-analysis examined the rates of anxiety and depression in adults with ASD and the impact of factors such as assessment methods and presence of comorbid intellectual disability (ID) diagnosis on estimated prevalence rates. Electronic database searches for studies published between January 2000 and September 2017 identified a total of 35 studies, including 30 studies measuring anxiety (n = 26 070; mean age = 30.9, s.d. = 6.2 years) and 29 studies measuring depression (n = 26 117; mean age = 31.1, s.d. = 6.8 years). The pooled estimation of current and lifetime prevalence for adults with ASD were 27% and 42% for any anxiety disorder, and 23% and 37% for depressive disorder. Further analyses revealed that the use of questionnaire measures and the presence of ID may significantly influence estimates of prevalence. The current literature suffers from a high degree of heterogeneity in study method and an overreliance on clinical samples. These results highlight the importance of community-based studies and the identification and inclusion of well-characterized samples to reduce heterogeneity and bias in estimates of prevalence for comorbidity in adults with ASD and other populations with complex psychiatric presentations

Advanced glycation end products (AGEs) in diabetic complications

Hyperglycemic condition in diabetes accelerates formation of advanced glycation end products (AGEs) that are formed as a result of series of reaction between reducing sugars and proteins. Accumulation of AGEs has been implicated in development of insulin resistance as well as in the pathogenesis of diabetic complications. The principal mechanism by which AGEs render harmful effects is through interaction with cell bound receptors. Certain receptors like AGE-R1 are involved in degradation of AGEs, while certain other receptors like receptor for AGE (RAGE) bring about counter effects exacerbating the situation. Accumulation of diverse AGEs, synergistically down regulate AGE-R1 while up regulate RAGE causing vicious cycle leading to enhanced formation and further accumulation of AGEs. In this article we discuss the formation of heterogeneous AGEs, importance of detection and quantification of AGEs, biological degradation of AGEs via different receptors, AGE-RAGE and its role in proinflammatory signaling, AGE mediated diabetic vascular complications such as nephropathy, retinopathy, neuropathy, cardiovascular and cerebrovascular diseases and finally the biological inhibition of AGEs is discussed along with chemical inhibitors for AGEs and natural products in AGE inhibition as a measure for the prevention of diabetic complications