期刊
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
卷 64, 期 9, 页码 743-753出版社
OXFORD UNIV PRESS INC
DOI: 10.1097/01.jnen.0000178444.33972.e0
关键词
Alzheimer; amyloid; amyloid precursor protein (APP); apoptosis; inflammation; microglia; necrosis; phagocytosis
资金
- NIA NIH HHS [AG 18478, AG 15490] Funding Source: Medline
- NINDS NIH HHS [NS 48335] Funding Source: Medline
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS048335] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R01AG018478, R01AG015490] Funding Source: NIH RePORTER
The presence of activated microglia in postmortem Alzheimer disease specimens is used to support the argument that inflammation contributes to Alzheimer pathogenesis. Transgenic mice overexpressing the amyloid precursor protein (APP) gene form amyloid plaques that are accompanied by local activation of microglia/macrophages in a manner similar to the human disease. Many markers of microglial activation and inflammation increase in an age-dependent manner in these mice. However, manipulation of these inflammatory reactions can lead to unexpected outcomes with several instances of reduced pathology when microglia/macrophages are activated further. In particular, anti-A beta immunotherapy in amyloid-depositing transgenic mice causes a complex series of changes in microglial markers, negating the implicit belief that such activation is monotonic and represented equally well by any of several activation markers. A survey of the peripheral macrophage literature identifies at least 2 distinct activation states of macrophages with different consequences for the surrounding tissue. These different activation states can often be distinguished by the markers that are expressed. Several markers are identified from studies outside the brain that neuroscientists might consider evaluating when attempting to more definitively describe the activation state of the monocyte-derived cells in the brain.
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