TY - JOUR
T1 - Inflammatory mechanisms in neurodegeneration.
AU - Nichols, Michael R.
AU - St‐Pierre, Marie‐Kim
AU - Wendeln, Ann‐Christin
AU - Wendeln, Ann‐Christin
AU - Makoni, Nyasha J.
AU - Gouwens, Lisa K.
AU - Garrad, Evan C.
AU - Sohrabi, Mona
AU - Neher, Jonas J.
AU - Neher, Jonas J.
AU - Tremblay, Marie‐Eve
AU - Combs, Colin K.
N1 - Michael R. Nichols Corresponding Author E-mail address: [email protected] https://orcid.org/0000-0001-5458-218X Department of Chemistry & Biochemistry, University of Missouri‐St. Louis, St. Louis, Missouri, USA Address correspondence and reprint requests to Dr Michael R. Nichols, Department of Chemistry & Biochemistry, University of Missouri‐St. Louis, One University Boulevard, St. Louis, MO, USA.
PY - 2019/6/1
Y1 - 2019/6/1
N2 - This review discusses the profound connection between microglia, neuroinflammation, and Alzheimer's disease (AD ). Theories have been postulated, tested, and modified over several decades. The findings have further bolstered the belief that microglia‐mediated inflammation is both a product and contributor to AD pathology and progression. Distinct microglia phenotypes and their function, microglial recognition and response to protein aggregates in AD , and the overall role of microglia in AD are areas that have received considerable research attention and yielded significant results. The following article provides a historical perspective of microglia, a detailed discussion of multiple microglia phenotypes including dark microglia, and a review of a number of areas where microglia intersect with AD and other pathological neurological processes. The overall breadth of important discoveries achieved in these areas significantly strengthens the hypothesis that neuroinflammation plays a key role in AD . Future determination of the exact mechanisms by which microglia respond to, and attempt to mitigate, protein aggregation in AD may lead to new therapeutic strategies.
AB - This review discusses the profound connection between microglia, neuroinflammation, and Alzheimer's disease (AD ). Theories have been postulated, tested, and modified over several decades. The findings have further bolstered the belief that microglia‐mediated inflammation is both a product and contributor to AD pathology and progression. Distinct microglia phenotypes and their function, microglial recognition and response to protein aggregates in AD , and the overall role of microglia in AD are areas that have received considerable research attention and yielded significant results. The following article provides a historical perspective of microglia, a detailed discussion of multiple microglia phenotypes including dark microglia, and a review of a number of areas where microglia intersect with AD and other pathological neurological processes. The overall breadth of important discoveries achieved in these areas significantly strengthens the hypothesis that neuroinflammation plays a key role in AD . Future determination of the exact mechanisms by which microglia respond to, and attempt to mitigate, protein aggregation in AD may lead to new therapeutic strategies.
UR - https://onlinelibrary.wiley.com/doi/full/10.1111/jnc.14674
U2 - 10.1111/JNC.14674
DO - 10.1111/JNC.14674
M3 - Article
VL - 149
JO - Journal of Neurochemistry
JF - Journal of Neurochemistry
ER -