Department of Psychiatry and Psychology, Mayo Clinic, Jacksonville, FL, USA.
Department of Psychiatry, Yokohama City University Medical Center, Yokohama, Japan.
Alzheimers Dement. 2018 Mar;14(3):330-339. doi: 10.1016/j.jalz.2017.09.014. Epub 2017 Oct 31.
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).
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.
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.
In DLB, α-synuclein is an important predictor of disease duration, both independently and synergistically with tau and Aβ.
我们旨在评估边缘和新皮质α-突触核蛋白、tau 和淀粉样蛋白 β（Aβ）对路易体痴呆（DLB）患者疾病持续时间的个体和综合贡献。
对 49 例临床可能的 DLB 患者的边缘和新皮质 α-突触核蛋白、tau 和 Aβ 进行定量数字病理学评估。回归模型检查了每种病理学对疾病持续时间方差的独特和共同贡献。
弥漫性路易体病患者的每种类型的病理学都更严重，疾病持续时间更短，而过渡性路易体病患者则更严重。这三种病理学共解释了疾病持续时间总方差的 25%，其中α-突触核蛋白单独或与 tau 和 Aβ 联合解释了 19%。当单独检查弥漫性路易体病组时，α-突触核蛋白沉积明显超过 tau 和 Aβ。在该模型中，α-突触核蛋白独立解释了疾病持续时间模型总方差的 24%中的 20%。
在 DLB 中，α-突触核蛋白是疾病持续时间的重要预测因子，无论是独立的还是与 tau 和 Aβ 协同的。
