Interestingly, this mechanism not only might be operative with Aβ and TAU [39] in AD but also to other neurodegenerative disorders such as α-synuclein (in Parkinson’s disease), Huntingtin protein (in Huntington’s disease), and islet amyloid polypeptide (IAPP, amylin) in the pancreas most probably through a common mechanism, in which EGCG binds to cross-beta sheets amyloid aggregation intermediates remodeling the oligomeric amyloid or pre-formed amyloid fibrils into non-amyloidogenic species [21,40]. This evidence concerns the gene HTT and Alzheimer disease.