
Oral infection with Porphyromonas gingivalis induced Alzheimer's disease (AD)-like lesions through the gut-brain axis. The infection led to alveolar resorption, gut microbiota dysbiosis, and impaired intestinal barrier function. Increased levels of 3-hydroxykynurenine in serum and hippocampi suppressed Bcl2 gene expression, promoting neuronal apoptosis. These findings suggest that P. gingivalis contributes to AD pathogenesis via alterations in the gut microbiota and tryptophan metabolism, offering new avenues for AD prevention and treatment.
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