Abstract
Abstract Alzheimer’s disease (AD) is the leading cause of dementia among older adults. AD is characterized by amyloid-β deposition, abnormal hyperphosphorylation of tau leading to the formation of neurofibrillary tangles, and neuroinflammation. Porphyromonas gingivalis, the keystone-pathogen of periodontitis, is being increasingly linked with AD and Alzheimer’s disease-related dementias (ADRD). Poor oral health is common in older populations, and literature suggests that oral health correlates with prevalence of ADRD. NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome-mediated IL-1β is significantly involved in periodontal diseases. However, the exact mechanism by which NLRP3 inflammasome is regulated in response to pathogenic bacteria remains unclear. We hypothesized that P. gingivalis-LPS may be responsible for the neuroinflammation via TLR4 activation and its downstream caspase-1, caspase-3 or caspase-4/5/11 dependent cell signaling. Our results suggest that P. gingivalis accelerated the induction of NLRP3. Furthermore, NLRP3/Caspase-1/Caspase-4/5/11 dependent IL-1β production may contribute to the dysregulated neuroinflammatory response in AD pathogenesis.
Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
