Basic Science and Pathogenesis.

Background: Age-related decrease glucose utilization, coupled with insulin resistance, are key features of AD, resulting in reduced glucose utilization/catabolism and oxidative stress generation. Irisin, an exercise-induced hormone promoting mitochondrial biogenesis in adipocytes via PGC-1α, stimulates thermogenic pathways, increases energy expenditure and induces browning of adipose tissue. Further, irisin expression was shown to trigger neuroprotection in AD models.

Method: Here, we assessed whether irisin could prevent potential metabolic deficits induced by soluble Aβ oligomers (AβOs) in hippocampal slices and in C57BL/6 mice.

Result: Our results indicate that irisin produced only subtle changes in the metabolic profile without clearly altering the protein content associated with mitochondrial dynamics in the AβOs-exposed hippocampus.

Conclusion: Our data suggest that other mechanisms may possibly contribute to the neuroprotective effects of irisin in AD models.