• S Zaheer, R Thangavel, S K Sahu, and A Zaheer.
• Department of Neurology, The University of Iowa, Iowa City, IA 52242, USA. asgar-zaheer@uiowa.edu
• Neuroscience. 2011 Oct 27; 194: 227233227-33.

AbstractWe have previously demonstrated that glia maturation factor (GMF), a brain-specific protein, isolated, sequenced, and cloned in our laboratory, is a prominent mediator of inflammation in the CNS leading to the death of neurons. In the present study, we demonstrate, for the first time, a significant upregulation of the GMF protein in various regions of Alzheimer's disease (AD) brains compared with age-matched non-demented (ND) control brains. We analyzed AD and ND brain samples by quantitative enzyme-linked immunosorbent assay (ELISA) using a combination of highly specific monoclonal and polyclonal anti-GMF antibodies developed and characterized in our laboratory. For the comparison between ND controls and AD cases, we examined brain tissue from 12 ad cases (ages ranging from 78-92 years) and eight age-matched ND controls (ages ranging from 76-88 years). We observed a significant increase in GMF concentration in entorhinal cortex, parietal cortex, frontal cortex, occipital cortex, perirhinal cortex, and temporal cortex of AD patients. Our results clearly demonstrate that the GMF protein levels are significantly higher in all AD-affected brain regions than in ND controls. The immunohistochemistry analysis revealed co-localization of GMF with amyloid plaques (AP) and neurofibrillary tangles (NFTs) in AD brains. Our results imply that under conditions of neurodegeneration the expression of GMF is significantly upregulated.Published by Elsevier Ltd.

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