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Modern societies face the increasing burden of agerelated diseases, in particular Alzheimer’s disease (AD) and type 2 diabetes (T2D). While numerous epidemiological studies have described the incidence of both diseases in the Western world and extensively defined common environmental risk factors,only little is known on the pathomechanisms linking both diseases [1–3]. Thus, it is not yet clear whether both diseases represent the endpoint of aged, exhausted, and dysfunctional cells having reached their maximal life expectancy or whether AD and T2D are the consequences of living in superabundance including excessive food supply, work demands, psychosocial stress, and an excessive sedentary life style [4–9]. Evidence for the latter is provided by the fact that high adiposity increases the risk of AD [10–12] and T2D [10,13] and implies that the progressive loss of energy balance is one underlying pathomechanism of both diseases. Interestingly, mammalian hibernators such as ground squirrels and hamsters demonstrate comparable and annual recurrent periods of obesity with concomitant insulin resistance and key features of AD such as tau phosphorylation [14,15]. These pathologies, however, are reversed by a time-dependent metabolic shift be-

The Alzheimer's Disease-Diabetes Angle: Inevitable Fate of Aging or Metabolic Imbalance Limiting Successful Aging