Targeting mitochondria in Alzheimer’s disease: effects of omega 3 fatty acids
Increasing evidences suggest that mitochondrial dysfunction plays an important role in the pathogenesis of neurodegenerative diseases including Alzheimer’s disease (AD). Alterations of mitochondrial efficiency and function are mainly related to failure of enzyme activities of mitochondrial complexes from the electron transport chain leading to oxidative stress, deficits in cellular bioenergetics and finally neuronal death. More recently, structural changes of the mitochondrial network were related to bioenergetic dysfunction, and the consequences are a matter of intensive research. The essential role of mitochondrial bioenergetics and the unique trajectory of alterations in brain metabolic capacity enable a bioenergetic- centric strategy that targets disease-stage specific pattern of brain metabolism for disease prevention and treatment. Recently, high fish intake or dietary supplementation with omega-3 fatty acids (n-3 FAs) has been linked to reductions in the risk of developing AD and to delayed cognitive decline in patients with very mild AD. However, the underlying cellular and molecular effects of n-3 FAs are poorly described. Here, we present new data demonstrating protective effects of n-3 FAs on bioenergetic function. Since mitochondrial dysfunction represents an early event in disease progression, more studies are needed that focus on therapeutic strategies starting before severe progression of the disease.