Editorial: Metabolism in Alzheimer's Disease

Fluorodeoxyglucose positron emission tomography (FDG-PET) comparing AD and CN individuals reveals lower glucose levels in the brains of AD patients (Herholz et al., 2002; Mosconi et al., 2010a; Marcus et al., 2014; Suppiah et al., 2019). Apolipoprotein E (APOE), the strongest genetic risk factor for sporadic AD, is both central to lipid metabolism and has been found to interact with inherited mitochondrial genes to amplify risk for AD (Carrieri et al., 2001; Andrews et al., 2020; Swerdlow et al., 2020). [...]molecular studies of AD brain show an overall reduction in the number of intact mitochondria and mitochondrial DNA (Swerdlow, 2018; Wilkins and Swerdlow, 2021). [...]mitochondrial function/dysfunction plays a role in protein aggregation, inflammation, and cell death; all events observed in AD. The authors focus on nuances for targeting mTOR in therapies including specificity for disease/region/and timing, pleiotropy, personalized therapy with relation to the effects of genetic factors, and the role of lifestyle factors and interventions.