Microglia mediated by SuM-ABN axis restores cognitive dysfunction and postones AD progression

• Published in: BIO web of conferences Vol. 166; p. 1004
• Main Author: Zhang, Xinyi
• Format: Journal Article Conference Proceeding
• Language: English
• Published: Les Ulis EDP Sciences 01.01.2025
• Subjects: Brain-derived neurotrophic factor; Cognitive ability; Immunosurveillance; Inflammation; Microglia; Neurogenesis; Phagocytosis; Phenotypes; Senile plaques; Stimulation
• ISSN: 2117-4458; 2273-1709; 2117-4458
• DOI: 10.1051/bioconf/202516601004

Microglia, a kind of highly dynamic central neural system immunity cells, transform phenotype based on diverse stimuli, playing vital roles in adult neurogenesis and synaptic connection for affecting AD progression. Particularly, microglia are mainly composed of anti-inflammatory types in mild AD patients, which offer immune surveillance to clear away amyloid beta plaques and facilitate adult neurogenesis. However, these microglia transform into pro-inflammatory alike phenotype to accelerate the deterioration of the disease if exposed to chronic but slow-level plaques stimulation. Thus, how to control microgial prototype becomes a promising therapeutic direction. It has been found that adult-born neurons activation mediated by SuM stimulation in early AD mice could promote microglia phagocytosis, improving cognitive functions. In this paper, I focus on whether microglia promote AHN by increasing BDNF release after SuM-ABN activation and whether chronic ABN-stimulated microglia could transform or maintain anti-inflammatory phenotype to prevent improper synaptic cut, leading to cognitive enhancement.