Semantic Scholar Open Access 2018 1341 sitasi

Microglia in Alzheimer’s disease

David V. Hansen Jesse E. Hanson Morgan Sheng

Abstrak

Proliferation and activation of microglia in the brain, concentrated around amyloid plaques, is a prominent feature of Alzheimer’s disease (AD). Human genetics data point to a key role for microglia in the pathogenesis of AD. The majority of risk genes for AD are highly expressed (and many are selectively expressed) by microglia in the brain. There is mounting evidence that microglia protect against the incidence of AD, as impaired microglial activities and altered microglial responses to &bgr;-amyloid are associated with increased AD risk. On the other hand, there is also abundant evidence that activated microglia can be harmful to neurons. Microglia can mediate synapse loss by engulfment of synapses, likely via a complement-dependent mechanism; they can also exacerbate tau pathology and secrete inflammatory factors that can injure neurons directly or via activation of neurotoxic astrocytes. Gene expression profiles indicate multiple states of microglial activation in neurodegenerative disease settings, which might explain the disparate roles of microglia in the development and progression of AD pathology.

Topik & Kata Kunci

Penulis (3)

D

David V. Hansen

J

Jesse E. Hanson

M

Morgan Sheng

Format Sitasi

Hansen, D.V., Hanson, J.E., Sheng, M. (2018). Microglia in Alzheimer’s disease. https://doi.org/10.1083/jcb.201709069

Akses Cepat

Lihat di Sumber doi.org/10.1083/jcb.201709069
Informasi Jurnal
Tahun Terbit
2018
Bahasa
en
Total Sitasi
1341×
Sumber Database
Semantic Scholar
DOI
10.1083/jcb.201709069
Akses
Open Access ✓