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Effect of apolipoprotein‐E Ε4 genotype on amyloid‐β and tau accumulation in Alzheimer’s disease
Author(s) -
Baek Min Seok,
Cho Hanna,
Lee Jae Hoon,
Ryu Young Hoon,
Lyoo Chul Hyoung
Publication year - 2020
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1002/alz.042284
Subject(s) - apolipoprotein e , pittsburgh compound b , cortex (anatomy) , amyloid (mycology) , posterior cingulate , medicine , alzheimer's disease , neuroscience , psychology , disease , pathology
Background We investigated effects of apolipoprotein E (ApoE) ε4 genotype on Aβ and tau burden and their longitudinal changes in Alzheimer’s disease spectrum. Method Among 272 individuals who underwent PET scans ( 18 F‐florbetaben for Aβ and 18 F‐flortaucipir for tau), and ApoE genotyping, 187 individuals completed 2‐year follow up PET scans. After correcting for partial‐volume effect, we compared the SUV ratio (SUVR) for Aβ and tau burden between ε4+ and ε4‐ groups. By using a linear mixed‐effect model, we measured the changes in SUVR in ApoE ε4+ and ε4‐ groups. Result ε4+ group showed greater baseline Aβ burden in diffuse cortical regions, and greater tau burden in lateral, and medial temporal, cingulate, and insula cortices. An annual accumulation rates of tau was higher in parietal, occipital, lateral and medial temporal cortices in ε4+ group. However, the accumulation of Aβ was not significantly different between ε4+ and ε4‐ groups. In Aβ+ individuals, baseline tau burden was higher in medial temporal cortex, while Aβ burden was conversely greater in ε4‐ group than ε4+ group in the global cortex, sensorimotor, and parietal cortices. Baseline Aβ burden showed decreasing trend and tau burden showed increasing trend associated with the number of ε4 alleles in dose‐dependent manner in Aβ+ individuals. Conclusion Progressive tau accumulation occurs in ε4 carriers in AD spectrum especially in medial and lateral temporal cortices. Existence of ε4 may modulate Aβ and tau burden differently based on the amount of existing amyloidosis.