Alzheimer’s disease progresses from the slow accumulation of amyloid-β plaques, that appear to cause comparatively mild dysfunction, to the accumulation of neurofibrillary tangles composed of altered tau protein, which cause major dysfunction and cell death in the later stages of the condition. Along the way chronic inflammation in brain tissue arises, along with dysfunctional behavior on the part of immune cells in the brain. As is the case in the open access review paper here, one can take these facts and suggest that amyloid-β deposition causes immune cell dysfunction, which in turn causes tau deposition. There is certainly evidence to support this view, such as the recent studies showing that clearance of senescent microglia turns back tau pathology and inflammation in animal models of Alzheimer’s disease. This is probably just one of several lines of cause and consequence, however: Alzheimer’s is a very complex condition.
Neuroinflammation is considered one of the cardinal features of Alzheimer’s disease (AD). Neuritic plaques composed of amyloid β and neurofibrillary tangle-laden neurons are surrounded by reactive astrocytes and microglia. Exposure of microglia, the resident myeloid cell of the central nervous system (CNS),
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