Review Article The Triggering Receptor Expressed on Myeloid Cells 2: ‘‘TREM-ming’ ’ the Inflammatory Component Associated with Alzheimer’s Disease

Copyright © 2013 Troy T. Rohn.This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Alzheimer’s disease (AD) is an age-related neurodegenerative disorder characterized by a progressive loss of memory and cognitive skills. Although much attention has been devoted concerning the contribution of the microscopic lesions, senile plaques, and neurofibrillary tangles to the disease process, inflammation has long been suspected to play a major role in the etiology of AD. Recently, a novel variant in the gene encoding the triggering receptor expressed on myeloid cells 2 (TREM2) has been identified that has refocused the spotlight back onto inflammation as amajor contributing factor in AD. Variants in TREM2 triple one’s risk of developing late-onset AD. TREM2 is expressed onmicroglial cells, the residentmacrophages in the CNS, and functions to stimulate phagocytosis on one hand and to suppress cytokine production and inflammation on the other hand.The purpose of this paper is to discuss these recent developments including the potential role that TREM2 normally plays and how loss of functionmay contribute to AD pathogenesis by enhancing oxidative stress and inflammation within the CNS. In this context, an overview of the pathways linking beta-amyloid, neurofibrillary tangles (NFTs), oxidative stress, and inflammation will be discussed. 1. Defining Alzheimer’s Disease Alzheimer’s disease (AD) is classified as a neurodegenerative disorder affecting neurons of the brain that are responsible fo