期刊
NATURE REVIEWS NEUROSCIENCE
卷 16, 期 6, 页码 358-372出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nrn3880
关键词
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资金
- Deutsche Forschungsgemeinschaft [SFB TRR 43, NeuroCure Exc 257, HE 3130/6-1]
- Federal Ministry of Education and Research (DLR/BMBF)
- European Union ITN-NeuroKine project
- Berlin Institute of Health (BIH)
- U. S. National Institutes of Health
- National Multiple Sclerosis Society
- Williams Family Fund for MS Research
- Guthy Jackson Charitable Foundation
- Swiss National Science Foundation [316030_150768, 310030_146130, CRSII3_136203]
- European Union
- university research priority project translational cancer research
- Swiss National Science Foundation (SNF) [CRSII3_136203] Funding Source: Swiss National Science Foundation (SNF)
The past two decades of research into the pathogenesis of Alzheimer disease (AD) have been driven largely by the amyloid hypothesis; the neuroinflammation that is associated with AD has been assumed to be merely a response to pathophysiological events. However, new data from preclinical and clinical studies have established that immune system-mediated actions in fact contribute to and drive AD pathogenesis. These insights have suggested both novel and well-defined potential therapeutic targets for AD, including microglia and several cytokines. In addition, as inflammation in AD primarily concerns the innate immune system - unlike in 'typical' neuroinflammatory diseases such as multiple sclerosis and encephalitides - the concept of neuroinflammation in AD may need refinement.
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