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 a major contributing factor in AD. Variants in TREM2 
triple one's risk of developing late-onset AD. TREM2 is expressed on microglial 
cells, the resident macrophages 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 function may 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.