Is there a link between genetic defects in the complement cascade and Porphyromonas gingivalis in Alzheimer's disease?

摘要: Defects, as determined by Genome-Wide Association Studies (GWAS), in the complement cascade of innate immunity have been suggested to play a key role Alzheimer's disease (AD). These defective genes encode sub-component 1s (C1s), receptor 1, component 9, and clusterin, fluid-phase regulatory protein. A dysregulated has shown relate cell activation, mediated clearance possible cognitive decline AD patients. Porphyromonas gingivalis, putative keystone pathogen periodontal disease, reported be associated with human AD. The inflammatory burden following experimental oral infection mice entry this bacterium into brain appears drive formation amyloid-beta plaques neurofibrillary tangles loss cognition. P. gingivalis is master immune subversion may establish microbial dysbiosis where it located. Here we discuss if enhance detrimental effects GWAS protein genes.