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Parkinson's disease dementia: convergence of α-synuclein, tau and amyloid-β pathologies.

机译:帕金森氏病痴呆症:α-突触核蛋白,tau和淀粉样蛋白-β病理学趋同。

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摘要

Dementia is increasingly being recognized in cases of Parkinson's disease (PD); such cases are termed PD dementia (PDD). The spread of fibrillar α-synuclein (α-syn) pathology from the brainstem to limbic and neocortical structures seems to be the strongest neuropathological correlate of emerging dementia in PD. In addition, up to 50% of patients with PDD also develop sufficient numbers of amyloid-β plaques and tau-containing neurofibrillary tangles for a secondary diagnosis of Alzheimer's disease, and these pathologies may act synergistically with α-syn pathology to confer a worse prognosis. An understanding of the relationships between these three distinct pathologies and their resultant clinical phenotypes is crucial for the development of effective disease-modifying treatments for PD and PDD.
机译:帕金森氏病(PD)病例中越来越多地认识到痴呆症;这种情况被称为PD痴呆症(PDD)。纤维性α-突触核蛋白(α-syn)病理学从脑干向边缘和新皮层结构的扩散似乎是PD中新出现的痴呆症的最强神经病理学关联。此外,多达50%的PDD患者还发展出足够数量的淀粉样蛋白β斑块和含有tau的神经原纤维缠结,可对阿尔茨海默氏病进行二次诊断,这些病理可能与α-syn病理协同作用,预后更差。 。了解这三种不同病理及其产生的临床表型之间的关系对于开发有效的PD和PDD疾病缓解疗法至关重要。

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