llular accumulation of diffuse and neuritic amyloid
plaques, composed of amyloid-b (Ab) peptide, and
frequently surrounded by dystrophic neurites and the intraneuronal
accumulation of neurofibrillary tangles (NFTs)
composed of hyperphosphorylated protein tau (p-tau)
[6,7]. These pathologic features are accompanied by
gliosis and the loss of neurons and synapses [7]. Although,
some studies reported a larger neuropathologic burden [8]
or a more widespread pathology extending outside the
medial temporal lobe in younger patients [5], overall the pathologic features of EOAD and LOAD patients are
largely similar, indicating that at the end-stage of disease,
it is difficult to distinguish the two AD age groups by
any other criterion than onset age