Alzheimer's disease (AD) is characterized by a marked desarborization of synaptic contacts and neuronal loss, leading to progressive memory deficits and cognitive decline [1]. Pathological changes in the brain, namely intracellular aggregates of tau protein filaments (neurofibrillary tangles) and extracellular deposition of beta amyloid peptides (amyloid plaques), constitute the hallmarks of the disease [2]. The search for biomarkers or early biological signs of AD has revealed genetic alterations as important risk factors for developing the disease, in particular the presence of the epsilon 4 allele of the apolipoprotein E (APOE-4) gene [3]–[7]. In addition, neuroimaging studies have provided substantial evidence indicating that atrophy and dysfunction in brain regions subserving cognitive function are closely associated with pathological aging or with the presence of the APOE-4 allele [8], [9].
