Year: 2024
Type: article
Abstract: Alzheimer's disease is associated with widespread expression of the C-X-C chemokine ligand (CXCL) 1 and its receptor, C-X-C chemokine receptor (CXCR) 2. The surface of neutrophils and monocytes/macrophages expresses CXCR2. Through the CXCL1/CXCR2 axis, these cells can be attracted to the lesion to take part in the inflammatory response. By activating certain neuronal pathways via the CXCL1/CXCR2 axis, CXCR2 expression in neurons will harm neurons. Astrocytes also express CXCR2, and when the receptor is active, the quantity of astrocytes increases but their functionality is compromised. Understanding the mechanisms underlying the CXCR2 impact during the progress of Alzheimer's disease may offer an appealing target for therapeutic therapy, as inflammation can arise at virtually any location of damage. The primary functions of CXCR2 in Alzheimer's disease are summarized in this review. CXCR2 affects the expression of Tau and Aβ, which may work in concert through microglial cells to cause Alzheimer's disease. The primary pathology associated with Alzheimer's disease is the accumulation of Tau and Aβ proteins. CXCR2's main functions in Alzheimer's disease are classified into the blood-brain barrier (BBB) disruption, γ-secretase, and neuroinflammation pathway, CXCR2 influences the production of Aβ protein in Alzheimer's disease. Additionally, it impacts Tau protein expression in Alzheimer's disease via the GSK 3 β and ERK/MAPK pathways.
DOI: 10.54097/ftb56d53
Author: Dongxu Qin
Institution: Monash University
Language: English
Subfield: Physiology
Field: Medicine
Domain: Health Sciences
Open Access status: diamond
OpenAlex ID: W4405809164