Glia Maturation Factor‐Antibody Injection Reduces Behavioral Impairment, Neuro Inflammation and Amyloid Pathology in 5XFAD Mice Brains

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by the accumulation of beta‐amyloid (Aβ) plaques and neurofibrillary tangles (NFTs) in the brain. Emerging evidence suggested that in neurodegenerative disease, aggregation of these proteins can promotes neuroinflammation and neurodegeneration. Glia maturation factor (GMF), a neuroinflammatory protein isolated and cloned in our laboratory play an important role in the pathogenesis of AD. To study the relationship between overexpression of GMF, glial activation and neuroinflammation, we used 9‐month‐old 5XFAD mice, a transgenic model of AD. We intravenously (iv) injected single dose of GMF antibody and found that antibody injection leads to: improvements in behavioral deficits, decreased activation of glial cells and reduced expression of pro‐inflammatory cytokines and amyloid pathology. We report that aberrant expression of GMF, GFAP, IBA1, and co‐localization of GMF with GFAP, IBA1 and Aβ significantly more in 5XFAD mice as compared with wild type mice. However, following GMF antibody injection, we found significant reduced expression of GMF, GFAP, IBA1 and Aβ in the cortex region of 5XFAD mice. We conclude that GMF‐antibody may be used to reduce neuroinflammation in neurodegenerative diseases including Alzheimer's disease.Support or Funding InformationNational Institutes of Health Grants NS073670, AG048205 and Veterans Affairs Merit Award I01BX002477 to AZ.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.