Journal
BRITISH JOURNAL OF PHARMACOLOGY
Volume 176, Issue 18, Pages 3515-3532Publisher
WILEY
DOI: 10.1111/bph.14618
Keywords
-
Categories
Funding
- Medical Research Council [MR/M024962/1, MC_EX_MR/N50192X/1, MR/L023784/1, MC_PC_16034, MR/L023784/2] Funding Source: Medline
- Parkinson's UK [J-0901] Funding Source: Medline
- Wellcome Trust Funding Source: Medline
- MRC [MR/L023784/2, MR/M024962/1, MC_PC_16034, MC_EX_MR/N50192X/1, MR/L023784/1] Funding Source: UKRI
Ask authors/readers for more resources
One of the largest unmet medical needs is a disease-modifying treatment for Alzheimer's disease (AD). Recently, the role of microglia in disease, particularly AD, has gained great interest, following the identification of several disease risk-associated genes that are highly expressed in microglia. Microglia play a critical homeostatic role in the brain, with neuroinflammatory and phagocytic mechanisms being of particular importance. Here, we review the role of NLRP3, the complement system, and the triggering receptor expressed in myeloid cells 2 (TREM2) in modulating microglial functions. We have reviewed the targets, their molecular pathways and the therapeutic interventions aimed at modulating these targets, in the hope of discovering a novel therapeutic approach for the treatment of AD. Linked Articles This article is part of a themed section on Therapeutics for Dementia and Alzheimer's Disease: New Directions for Precision Medicine. To view the other articles in this section visit
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available