LAUSR

Irisin is involved in various metabolic pathways and is suggested to be a potential agent capable of preventing onset of Alzheimer's disease (AD) and ameliorating AD neuropathology and cognitive deficits. In the present study, the serum levels of Irisin and Amyloid-β (Aβ) peptides and the neurocognitive performance among obese individuals at genetic risk for AD were investigated. The correlations between Irisin and AD-related neuropathological and neurocognitive indices were also explored. Thirty-two individuals with a family history of AD (ADFH) and obesity (ADFH-obesity group) and 32 controls (ADFH-non-obesity group) were recruited. Circulating levels of Irisin, Aβ peptides, and metabolic biomarkers, as well as neurocognitive performance [e.g., behavior and brain even-related potentials (ERP)] were measured during a visuospatial working memory task. Although the ADFH-obesity group exhibited comparable reaction times, ERP N2 latency and amplitudes, and P3 latency as compared to the ADFH-non-obesity group when performing the cognitive task, they exhibited significantly lower rates of accuracy and smaller P3 amplitudes in the higher memory-load condition, even when controlling for the blood pressure and cardiorespiratory fitness co-variables. The serum levels of leptin, insulin, and glucose, and HOMA-IR were significantly higher in the ADFH-obesity group relative to the ADFH-non-obesity group, but this was not the case for the levels of Aβ1-40 and Aβ1-42. The Irisin levels approached between-group significance. Partial correlations adjusting for cardiorespiratory fitness and blood pressure showed that Irisin levels were positively associated with neurophysiological (i.e., P3 amplitude) performance in the ADFH-obesity group. The Irisin levels were not significantly correlated with the levels of Aβ1-40 and Aβ1-42. ADFH individuals with obesity exhibited neurocognitive deficits when performing the visuospatial working memory task, and serum Irisin levels could be one of the influencing factors. However, the relationship between the circulating levels of Irisin Aβ peptides needs more evidence to support this assumption.