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

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

Alzheimers Dement. 2017 Oct 31;:

Authors: 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

Abstract
INTRODUCTION: 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 (DLB).
METHODS: Quantitative digital pathology of neocortical and limbic α-synuclein, tau, and β-amyloid 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 β-amyloid. When the diffuse Lewy body disease group was examined separately, α-synuclein deposition significantly exceeded that of tau and β-amyloid. 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 β-amyloid.

PMID: 29100980 [PubMed - as supplied by publisher]

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