TTR and Alzheimer disease: In silico and cell functional studies revealed four potentially pathogenic rare TTR variants in AD: c.-239C>A, which decreased TTR promoter activity; c.200+4A>G, which may influence TTR mRNA inherent splicing; and c.148G>A (p. V50M) and c.332C>T (p.A111V) which may change TTR structure and reduce Aβ binding affinity [11].