Journal of Neuroinflammation Interleukin-1 Mediates Alzheimer and Lewy Body Pathologies
Journal of Neuroinflammation Interleukin-1 Mediates Alzheimer and Lewy Body Pathologies
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通讯作者：
W. Sue;T. Griffin;Ling Liu;Yuekui Li;R. Mrak;S. Barger;Email W Sue;Yuekui;Robert
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作者：
W. Sue;T. Griffin;Ling Liu;Yuekui Li;R. Mrak;S. Barger;Email W Sue;Yuekui;Robert
背景：阿尔茨海默病（AD）和帕金森病（PD）的临床和神经病理重叠现已得到充分认识。这类AD合并路易体病（AD/ LBD）的病例表现为神经病理改变，包括路易体（α-突触核蛋白聚集体）、神经性淀粉样斑块和神经原纤维缠结（过度磷酸化的tau聚集体）。这些临床和神经病理变化的共同发生表明这些疾病的共同致病机制，以前被认为是不同的。神经胶质细胞的激活与白细胞介素-1 （IL-1）和其他促炎细胞因子的过度表达越来越多地与AD和PD的发病机制有关。
Background: Clinical and neuropathological overlap between Alzheimer's (AD) and Parkinson's disease (PD) is now well recognized. Such cases of concurrent AD and Lewy body disease (AD/ LBD) show neuropathological changes that include Lewy bodies (α-synuclein aggregates), neuritic amyloid plaques, and neurofibrillary tangles (hyperphosphorylated tau aggregates). The co-occurrence of these clinical and neuropathological changes suggests shared pathogenic mechanisms in these diseases, previously assumed to be distinct. Glial activation, with overexpression of interleukin-1 (IL-1) and other proinflammatory cytokines, has been increasingly implicated in the pathogenesis of both AD and PD.