The limbic and neocortical contribution of α-synuclein, tau, and amyloid β to disease duration in dementia with Lewy bodies.

The limbic and neocortical contribution of α-synuclein, tau, and amyloid β to disease duration in dementia with Lewy bodies.
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DOI:
10.1016/j.jalz.2017.09.014
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发表时间:
2018-03
期刊:
Alzheimer's & dementia : the journal of the Alzheimer's Association
影响因子:
--
通讯作者:
Dickson DW
Dickson DW
中科院分区:
其他
文献类型:
--
作者:
Ferman TJ;Aoki N;Crook JE;Murray ME;Graff-Radford NR;van Gerpen JA;Uitti RJ;Wszolek ZK;Graff-Radford J;Pedraza O;Kantarci K;Boeve BF;Dickson DW

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We sought to assess the individual and combined contribution of limbic and neocortical α-synuclein, tau and β-amyloid to duration of illness in dementia with Lewy bodies. Quantitative image analysis of neocortical and limbic α-synuclein, tau and β-amyloid was assessed in 49 patients with clinically probable dementia with Lewy bodies. Regression modelling examined the unique and shared contribution of each pathology to the variance of illness duration. Patients with diffuse Lewy body disease had more severe pathology of each type and a shorter duration of illness than individuals with transitional Lewy body disease. The three pathologies accounted for 25% of the total variance of duration of illness, with 19% accounted for by α-synuclein alone or in combination with tau and β-amyloid. When the diffuse Lewy body disease group was examined separately, α-synuclein deposition exceeded that of tau and β-amyloid, and survival was not related to differences in tau or β-amyloid burden. In this model, 20% of 24% total variance in the model for duration of illness was accounted for independently by α-synuclein. In dementia with Lewy bodies, the burden of α-synuclein is an important predictor of disease duration, both independently and synergistically with tau and β-amyloid.
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