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The limbic and neocortical contribution of α‐synuclein, tau, and amyloid β to disease duration in dementia with Lewy bodies
Author(s) -
Ferman Tanis J.,
Aoki Naoya,
Crook Julia E.,
Murray Melissa E.,
GraffRadford Neill R.,
Gerpen Jay A.,
Uitti Ryan J.,
Wszolek Zbigniew K.,
GraffRadford Jonathan,
Pedraza Otto,
Kantarci Kejal,
Boeve Bradley F.,
Dickson Dennis W.
Publication year - 2018
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 - 10.1016/j.jalz.2017.09.014
Subject(s) - lewy body , dementia with lewy bodies , dementia , parkinson's disease , disease , alpha synuclein , neuroscience , pathology , psychology , amyloid (mycology) , medicine
We sought to assess the individual and combined contribution of limbic and neocortical α‐synuclein, tau, and amyloid β (Aβ) to duration of illness in dementia with Lewy bodies (DLB). Methods Quantitative digital pathology of limbic and neocortical α‐synuclein, tau, and Aβ was assessed in 49 patients with clinically probable DLB. Regression modeling examined the unique and shared contribution of each pathology to the variance of illness duration. Results 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 Aβ. When the diffuse Lewy body disease group was examined separately, α‐synuclein deposition significantly exceeded that of tau and Aβ. In this model, 20% of 24% total variance in the model for duration of illness was accounted for independently by α‐synuclein. Discussion In DLB, α‐synuclein is an important predictor of disease duration, both independently and synergistically with tau and Aβ.