Abstract
AbstractBackgroundAtypical variants of Alzheimer's Disease (AD) manifest predominantly with non‐memory complaints, including visuospatial (posterior cortical atrophy), language (logopenic variant of primary progressive aphasia), motor (cortico‐basal syndrome), executive or cognitive‐behavioral patterns. Compared to typical (amnestic) AD, these atypical profiles are characterized by faster cognitive decline rates, syndrome‐specific atrophy patterns, younger age at onset, and tend to be less associated with apolipoprotein E (APOE) ɛ4 allele genotype.Despite clinical differences, both typical AD and atypical AD variants feature deposits of amyloid plaques and neurofibrillary tangles and can be staged using the same neuropathological guidelines. Although it is clear that AD atypical phenotypes presented different atrophy and hypometabolism patterns among themselves and compared to typical AD, it is unclear what is the neuropathological subtract underlying an atypical AD presentation. Our work, supported by the literature, suggests that the regional pattern of plaque accumulation in advanced disease is not distinctive in each of the clinical variants of AD. Conversely, cumulative evidence from neuropathology and neuroimaging studies suggests that variations in the regional tau burden are closely related to the expression of AD's clinical variants.MethodThis presentation will review published and unpublished evidence from human neuropathological studies addressing the neurobiological substrates atypical AD variantsResultIt will include a discussion on similarities and differences in plaque and tangle burden, neuropathological comorbidities. We will also present unpublished results from a systematic study with over 140 AD cases (35% atypical) showing that comorbid pathologies do not play an essential role in determining atypical ADConclusionFinally, it will discuss the role of distinct mechanisms of selective neuronal vulnerability in concern with atypical AD.
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