Repetitive Behaviors in Autism and Obsessive-Compulsive Disorder: A Systematic Review.

PURPOSE: Obsessive-compulsive disorder (OCD) and autism are characterized by the presence of repetitive behaviors. Differentiating between repetitive behaviors attributable to a diagnosis of autism, and those attributable to OCD, poses challenges for differential and co-occurring diagnosis. Differentiation is important to inform appropriate supports and interventions for phenotypically similar but functionally distinct behaviors. In this systematic review, the quantitative literature was examined to explore the similarities and differences in repetitive behaviors (including restricted and repetitive behaviors and interests, and obsessive-compulsive behaviors) in autistic individuals and those with OCD, and those with co-occurring diagnoses, in terms of: (1) expression, (2) content, and (3) associated factors. METHODS: Thirty-one studies were identified that compared repetitive behaviors in autistic individuals, individuals with OCD, or individuals with both diagnoses. RESULTS: The results suggest considerable overlap in the intensity and content of repetitive behaviors between groups. The findings of this review highlight that research aimed specifically at understanding similarities and differences in repetitive behaviors between autistic individuals and individuals with OCD is limited and frequently only compare at total score or composite measure levels. CONCLUSION: Further research into differences in the presentation of repetitive behaviors at a subscale and item level is required to inform clearer differentiation of specific behaviors in autism versus OCD. Understanding and more accurately differentiating is essential for efficient diagnosis, effective treatment, and better outcomes.

Amyloid beta 42 alters cardiac metabolism and impairs cardiac function in male mice with obesity.

There are epidemiological associations between obesity and type 2 diabetes, cardiovascular disease and Alzheimer's disease. The role of amyloid beta 42 (Aß42) in these diverse chronic diseases is obscure. Here we show that adipose tissue releases Aß42, which is increased from adipose tissue of male mice with obesity and is associated with higher plasma Aß42. Increasing circulating Aß42 levels in male mice without obesity has no effect on systemic glucose homeostasis but has obesity-like effects on the heart, including reduced cardiac glucose clearance and impaired cardiac function. The closely related Aß40 isoform does not have these same effects on the heart. Administration of an Aß-neutralising antibody prevents obesity-induced cardiac dysfunction and hypertrophy. Furthermore, Aß-neutralising antibody administration in established obesity prevents further deterioration of cardiac function. Multi-contrast transcriptomic analyses reveal that Aß42 impacts pathways of mitochondrial metabolism and exposure of cardiomyocytes to Aß42 inhibits mitochondrial complex I. These data reveal a role for systemic Aß42 in the development of cardiac disease in obesity and suggest that therapeutics designed for Alzheimer's disease could be effective in combating obesity-induced heart failure.