TY - JOUR
T1 - Association between Aβ and tau accumulations and their influence on clinical features in aging and Alzheimer's disease spectrum brains
T2 - A [11C]PBB3-PET study
AU - Shimada, Hitoshi
AU - Kitamura, Soichiro
AU - Shinotoh, Hitoshi
AU - Endo, Hironobu
AU - Niwa, Fumitoshi
AU - Hirano, Shigeki
AU - Kimura, Yasuyuki
AU - Zhang, Ming Rong
AU - Kuwabara, Satoshi
AU - Suhara, Tetsuya
AU - Higuchi, Makoto
N1 - Publisher Copyright:
© 2016 The Authors
PY - 2017
Y1 - 2017
N2 - Introduction Amyloid-β (Aβ) and tau accumulations may occur independently and concurrently as exemplified by primary age-related tauopathy and Alzheimer's disease (AD), respectively. Interactions between Aβ and tau accumulations and their influence on clinical features, however, are still unclear. Methods Associations among clinical symptoms, gray-matter volume, regional tau, and Aβ deposition assessed by positron emission tomography with [11C]pyridinyl-butadienyl-benzothiazole 3 (PBB3) and [11C]Pittsburgh compound-B (PiB), were evaluated in 17 AD, 9 mild cognitive impairment due to AD, and 28 PiB(−)-cognitive healthy controls (HCs). Results High tau burden was associated with aging and low-level education in PiB(−)-HC and AD-spectrum groups, and with high Aβ burden and low-level education in all subjects. It was not Aβ but tau accumulation that showed significant associations with cognitive performance even in PiB(−)-HC. Discussion The present study indicated aging and low-level education after Aβ would be enhancers for tau pathology, associated with neurodegeneration and cognitive impairment in healthy and diseased elderly individuals.
AB - Introduction Amyloid-β (Aβ) and tau accumulations may occur independently and concurrently as exemplified by primary age-related tauopathy and Alzheimer's disease (AD), respectively. Interactions between Aβ and tau accumulations and their influence on clinical features, however, are still unclear. Methods Associations among clinical symptoms, gray-matter volume, regional tau, and Aβ deposition assessed by positron emission tomography with [11C]pyridinyl-butadienyl-benzothiazole 3 (PBB3) and [11C]Pittsburgh compound-B (PiB), were evaluated in 17 AD, 9 mild cognitive impairment due to AD, and 28 PiB(−)-cognitive healthy controls (HCs). Results High tau burden was associated with aging and low-level education in PiB(−)-HC and AD-spectrum groups, and with high Aβ burden and low-level education in all subjects. It was not Aβ but tau accumulation that showed significant associations with cognitive performance even in PiB(−)-HC. Discussion The present study indicated aging and low-level education after Aβ would be enhancers for tau pathology, associated with neurodegeneration and cognitive impairment in healthy and diseased elderly individuals.
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U2 - 10.1016/j.dadm.2016.12.009
DO - 10.1016/j.dadm.2016.12.009
M3 - Article
AN - SCOPUS:85009837024
SN - 2352-8729
VL - 6
SP - 11
EP - 20
JO - Alzheimer's and Dementia: Diagnosis, Assessment and Disease Monitoring
JF - Alzheimer's and Dementia: Diagnosis, Assessment and Disease Monitoring
ER -