Regional neuronal compensation in early and late stages of the Alzheimer’s trajectory

Glucose hypermetabolism is suggested to occur as a compensatory response to early neuronal damage[1]. Hypermetabolism has been shown to arise in the prodromal phase of Alzheimer’s disease development as a mechanism to prevent against cognitive deficits or as a compensatory mechanism to maintain the neuronal function amidst of other neurodegenerative process. Here we aimed to evaluate whether there is regional glucose hypermetabolism as a proxy to neuronal function in response to tau deposition in different stages of Alzheimer’s disease.