GFAP and Alzheimer disease: The processes leading to protein aggregation are not well defined, but it is widely accepted that aggregates are initiated by oligomerization of seed proteins, which in AD are primarily Aβ1-42 and hyperphosphorylated tau (hP-tau) fragments [79] but may also include hyperphosphorylation of glial fibrillary acidic protein (GFAP) [27], α-synuclein [90], transactive response DNA-binding protein 43 (TDP-43) [89], and triggering receptor expressed on myeloid cells 2 (TREM2) [43].