Intermediated repeat expansions in ATXN2 (27-32Qs) are viewed as a genetic risk factor, as they modulate the pathogenesis and the age at onset of several other neurodegenerative diseases including transthyretin familial amyloid polyneuropathy (TTR-FAP), frontotemporal dementia (FTD), Alzheimer ́s disease (AD), corticobasal syndrome, ALS, and SCA3 [48–54]. Here, TTR is linked to early-onset autosomal dominant Alzheimer disease.