TY - JOUR
T1 - APOE ε4 influences medial temporal atrophy and tau deposition in atypical Alzheimer's disease
AU - Singh, Neha Atulkumar
AU - Tosakulwong, Nirubol
AU - Graff-Radford, Jonathan
AU - Machulda, Mary M.
AU - Pham, Nha Trang Thu
AU - Sintini, Irene
AU - Weigand, Stephen D.
AU - Schwarz, Christopher G.
AU - Senjem, Matthew L.
AU - Carrasquillo, Minerva M.
AU - Ertekin-Taner, Nilufer
AU - Jack, Clifford R.
AU - Lowe, Val J.
AU - Josephs, Keith A.
AU - Whitwell, Jennifer L.
N1 - Publisher Copyright:
© 2022 the Alzheimer's Association.
PY - 2023/3
Y1 - 2023/3
N2 - Introduction: Apolipoprotein E (APOE) ε4 is an important genetic risk factor for typical Alzheimer's disease (AD), influencing brain volume and tau burden. Little is known about its influence in atypical presentations of AD. Methods: An atypical AD cohort of 140 patients diagnosed with either posterior cortical atrophy or logopenic progressive aphasia underwent magnetic resonance imaging and positron emission tomography. Linear mixed effects models were fit to assess the influence of APOE ε4 on cross-sectional and longitudinal regional metrics. Results: At baseline, APOE ε4 carriers had smaller hippocampal and amygdala volumes and greater tau standardized uptake volume ratio in the hippocampus and entorhinal cortex compared to non-carriers while longitudinally, APOE ε4 non-carriers showed faster rates of atrophy and tau accumulation in the entorhinal cortex, with faster tau accumulation in the hippocampus. Discussion: APOE ε4 influences patterns of neurodegeneration and tau deposition and was associated with more medial temporal involvement, although there is evidence that non-carriers may be catching up over time.
AB - Introduction: Apolipoprotein E (APOE) ε4 is an important genetic risk factor for typical Alzheimer's disease (AD), influencing brain volume and tau burden. Little is known about its influence in atypical presentations of AD. Methods: An atypical AD cohort of 140 patients diagnosed with either posterior cortical atrophy or logopenic progressive aphasia underwent magnetic resonance imaging and positron emission tomography. Linear mixed effects models were fit to assess the influence of APOE ε4 on cross-sectional and longitudinal regional metrics. Results: At baseline, APOE ε4 carriers had smaller hippocampal and amygdala volumes and greater tau standardized uptake volume ratio in the hippocampus and entorhinal cortex compared to non-carriers while longitudinally, APOE ε4 non-carriers showed faster rates of atrophy and tau accumulation in the entorhinal cortex, with faster tau accumulation in the hippocampus. Discussion: APOE ε4 influences patterns of neurodegeneration and tau deposition and was associated with more medial temporal involvement, although there is evidence that non-carriers may be catching up over time.
KW - apolipoprotein ε4
KW - atypical Alzheimer's disease
KW - logopenic progressive aphasia
KW - magnetic resonance imaging
KW - posterior cortical atrophy
KW - tau positron emission tomography
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U2 - 10.1002/alz.12711
DO - 10.1002/alz.12711
M3 - Article
C2 - 35691047
AN - SCOPUS:85131551197
SN - 1552-5260
VL - 19
SP - 784
EP - 796
JO - Alzheimer's and Dementia
JF - Alzheimer's and Dementia
IS - 3
ER -