Britschgi Markus, Wyss-Coray Tony
Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305, USA.
Int Rev Neurobiol. 2007;82:205-33. doi: 10.1016/S0074-7742(07)82011-3.
Alzheimer's disease (AD) is a neurodegenerative disorder characterized clinically by a progressive cognitive decline and dementia. AD brains are marked by amyloid plaques and neurofibrillary tangles, neuronal cell loss, and a prominent activation of glial cells, and innate immune responses. A growing number of studies in AD have also reported alterations in systemic immune responses including changes in lymphocyte and macrophage distribution and activation, the presence of autoantibodies, or abnormal cytokine production. Studies in animal models for AD support the notion that immune cells infiltrate the brain and may modulate the disease. Here we will review evidence for systemic alterations in immune responses and a role for acquired immunity in AD and discuss their potential contribution to the disease.
阿尔茨海默病(AD)是一种神经退行性疾病,临床上以进行性认知衰退和痴呆为特征。AD患者的大脑具有淀粉样斑块、神经原纤维缠结、神经元细胞丢失以及胶质细胞和先天免疫反应的显著激活等特征。越来越多关于AD的研究还报告了全身免疫反应的改变,包括淋巴细胞和巨噬细胞分布及激活的变化、自身抗体的存在或细胞因子产生异常。对AD动物模型的研究支持免疫细胞浸润大脑并可能调节该疾病这一观点。在此,我们将综述免疫反应全身改变的证据以及获得性免疫在AD中的作用,并讨论它们对该疾病的潜在影响。