Ongoing studies of deimination in neurodegenerative diseases using the F95 antibody

Abstract

Over the past decade, growing evidence has emerged, suggesting that protein deimination is increased in human neurodegenerative disorders such as Alzheimer's disease, Creutzfeldt-Jakob disease, and Parkinson's disease. As an additional tool to identify affected proteins, some of these experiments utilized the F95 monoclonal antibody, which can theoretically recognize any protein in which arginine amino acids have been transformed to citrullines. This chapter outlines previous studies of brain protein deimination in these aforementioned maladies using F95 as well as ongoing unpublished studies of other neurodegenerative disorders such as Alexander's disease, amyotrophic lateral sclerosis, diffuse Lewy body disease, some primary astrocytic neoplasms, and normal brain aging. In addition, some data associated with the animal models of these conditions are also presented. Collectively, most of these conditions support the trending concept that neurodegeneration, for whatever reason, is accompanied by amplified citrullination, although the proteins affected and pattern of increased deimination in the central nervous system may differ in different disease states.