Tejera Dario, Heneka Michael T
Clinical Neuroscience Unit, Department of Neurology, University of Bonn. Sigmund Freud Strasse 25, 53127, Bonn, Germany.
Curr Alzheimer Res. 2016;13(4):370-80. doi: 10.2174/1567205013666151116125012.
Traditionally the brain has been viewed as being an immune-privileged organ. However, endogenous stimuli such as the presence of misfolded or aggregated proteins, as well as systemic inflammatory events may lead to the activation of microglial cells, the brain's innate immune system, and, subsequently, to neuroinflammation. Alzheimer's disease, the leading cause of dementia, is characterized by amyloid beta deposition and tau hyperphosphorylation. Neuroinflammation in Alzheimer's disease has been identified as major contributor to disease pathogenesis. Once activated, microglia release several pro and anti-inflammatory mediators of which several affect the function and structure of the brain. Modulation of this microglial activation in Alzheimer's disease might open new therapeutic avenues.
传统上，大脑被视为一个免疫特权器官。然而，内源性刺激，如错误折叠或聚集蛋白的存在，以及全身性炎症事件，可能会导致小胶质细胞（大脑的固有免疫系统）的激活，进而引发神经炎症。老年痴呆症是痴呆的主要病因，其特征是β-淀粉样蛋白沉积和tau蛋白过度磷酸化。老年痴呆症中的神经炎症已被确定为疾病发病机制的主要促成因素。一旦被激活，小胶质细胞会释放多种促炎和抗炎介质，其中一些会影响大脑的功能和结构。调节老年痴呆症中的这种小胶质细胞激活可能会开辟新的治疗途径。
