Alzheimer’s Disease and Porphyromonas gingivalis

Anti-Gingipain B (RgpB) MAb from QED Bioscience

Although the cause of Alzheimer’s  disease (AD) is still unknown, a long-standing, widely-accepted  hypothesis is that it is caused by the accumulation of misfolded proteins in the brain.  Unfortunately, drugs that target those misfolded proteins have failed in clinical trials to ameliorate the disease which leads us to question whether misfolded proteins are  symptoms or the cause of AD.  A recent and surprising alternative hypothesis is that AD might result from an infection by the oral  bacterium Porphyromonas gingivalis, the primary pathogen associated with chronic periodontal disease.  P. gingivalisproduces toxins called  gingipains, cysteine proteases that have been found in the brain and  cerebrospinal fluid of AD patients in association with neurons, tau tangles, and beta-amyloid.  Gingipains can degrade human  proteins – could they be responsible for the misfolded proteins associated with AD? Of great interest are studies in which oral administration of  P. gingivalis to mice led to AD-like  neurodegeneration and formation of amyloid plaque and neurofibrillary  tangles. Clinical trials of gingipain  inhibitors that look promising in mouse models are currently underway.

QED Bioscience is pleased to  introduce Anti-Gingipain B (RgpB) monoclonal antibody 18E6.F7 (#13925) for investigations into the link between P. gingivalis and AD.   It has been used successfully in IHC, WB, and ELISA to detect gingipain B.

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Anti-Gingipain B (RgpB) monoclonal antibody 18E6.F7