Overexpression and aberrant activation of GSK-3β are correlated with tau hyperphosphorylation (with its consequent dissociation from microtubules and aggregation into neurofibrillary tangles, NFTs), alteration of amyloid precursor protein (APP) processing and amyloid-β (Aβ)-induced neurotoxicity in AD, and increased α-synuclein expression in PD [17]. This evidence concerns the gene APP and Alzheimer disease.