By Ralph Sanchez, MTCM, CNS, D.Hom.
Recently (11/13), a rare variant of the TREM2 gene, designated as R47H, was shown to increase the risk of developing Alzheimer’s disease. Individuals with the variant may be up to 3 to 5 times more likely to develop late-onset Alzheimer’s disease (LOAD). This susceptibility to LOAD in R47H genotypes, is similar to that conferred by the ApoE4 gene.
The TREM2 gene is involved in immune regulatory processes in the brain and the R47H mutation impairs the gene’s ability to contain inflammation. One of the roles of the TREM2 gene that encodes for TREM 2 protein receptor on microglia, is to aid the brain in efficiently eliminating beta amyloid–the toxic protein that forms plaques associated with Alzheimer’s disease. (more…)
By Ralph Sanchez, L.Ac.,CNS,D.Hom.
The role of chronic inflammation in degenerative disease associated with aging is considered to be a primary vector for the progression of neurodegenative disorders and a powerful factor that underlies their etiology. One needs only to look at the leading causes of mortality, heart disease and stroke, and the research models of inflammation that clearly link it to the pathogenesis and the pathology of these disease processes to understand that inflammation and chronic degenerative disease are inseparable.
Since inflammation is central to aging-associated disease processes, it has been heavily investigated in models of neurodegeneration. In Alzheimer’s disease (AD), the investigation has sought to clarify whether inflammation is a causative stimulus, or a concomitant feature of the disease. Regardless of the etiological focus, the role of chronic inflammation in AD is a well established and the continuing illumination of that knowledge base is vital to the emerging paradigm that seeks to emphasize prevention over a pharmaceutical solution.