Table 3.

Genetic and molecular factors linked to the AD spectrum (see sections 3, 4 and 21 for references).

FAD	mutations in the genes APP, PSEN1 (presenilin1), and PSEN2; increased APP dosage
sAD	ε4 of ApoE, LRP1, LDLR, interleukin 1a, CLU, PICALM, CR1, BIN1, TREM2, SORL1, ADAM10, ABCA7, SPI1, PILRA, MSA4, CD2AP, and EPHA1
PART	lower prevalence of ApoEε4, PTK2B, BIN1, and CR1 genes, and higher prevalence of ApoEε2
rpAD	low frequency of ApoEε4 allele; increased inflammation; different Aβ oligomers; different amyloid‑β proteoforms; different seeding capacities of β-amyloid; high-density PrP oligomers; decreased PrP di-glycosylated isoforms; specific PrP isoform; altered localization of the growth arrest-specific 2-like 2 protein (G2L2), α-tubulin and β-actin; downregulation and dislocalization from the nucleus to the cytoplasm of SFPQ, their colocalization with TIA-1 in stress granules, and their association with tau oligomers
resilient AD	variant of chromosome 18 upstream of ATP8B1; rare variant in the 3'-UTR of RAB10; MEF2C upregulation in a subpopulation of glutamatergic neurons; decreased expression levels of chemokines and increased levels of trophic factors
Tangle-predominant dementia	association with MAPT H1 haplotype