Journal
NEURAL REGENERATION RESEARCH
Volume 18, Issue 4, Pages 763-768Publisher
WOLTERS KLUWER MEDKNOW PUBLICATIONS
DOI: 10.4103/1673-5374.354514
Keywords
beta-hydroxybutyrate; cytokines; HCAR2; lupus; neuroinflammation; neuropathic; niacin; nociception; synaptic
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Neuroinflammation is crucial in the development of various neurological disorders and pathological pain conditions. GPR109A, a Gi protein-coupled receptor, is identified as a significant therapeutic target for controlling inflammation in different tissues and organs. This review summarizes the current knowledge regarding the role of GPR109A in neuroinflammation, with a focus on its pharmacological features and signaling pathways involved in alleviating neuroinflammation and symptoms in Alzheimer's disease, Parkinson's disease, multiple sclerosis, stroke, and pathological pain conditions.
Neuroinflammation plays a critical role in the pathological process of multiple neurological disorders and pathological pain conditions. GPR109A, a Gi protein-coupled receptor, has emerged as an important therapeutic target for controlling inflammation in various tissues and organs. In this review, we summarized current data about the role of GPR109A in neuroinflammation. Specifically, we focused on the pharmacological features of GPR109A and signaling pathways used by GPR109A to ameliorate neuroinflammation and symptoms in Alzheimer's disease, Parkinson's disease, multiple sclerosis, stroke, and pathological pain conditions.
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