Noradrenergic signaling controls Alzheimer's disease pathology via activation of microglial β2 adrenergic receptors.

ABSTRACT: In Alzheimer's disease (AD) pathophysiology, plaque and tangle accumulation trigger an inflammatory response that mounts positive feed-back loops between inflammation and protein aggregation, aggravating neurite damage and neuronal death. One of the earliest brain regions to undergo neurodegeneration is the locus coeruleus (LC), the predominant site of norepinephrine (NE) production in the central nervous system (CNS). In animal models of AD, dampening the impact of noradrenergic signaling pathways, either through administration of beta blockers or pharmacological ablation of the LC, heightened neuroinflammation through increased levels of pro-inflammatory mediators. Since microglia are the resident immune cells of the CNS, it is reasonable to postulate that they are responsible for transl

SUBMITTER: Le L 

PROVIDER: S-EPMC10723313 | biostudies-literature | 2023 Dec

REPOSITORIES: biostudies-literature