Our work suggests that protein misfolding and immune activation in neurodegenerative disorders are triggered through cross-seeding by exposure to exogenous microbial amyloids in the nose, mouth and gut.
Streptococcus mutans, Staphlococcus aureus, Salmonella enterica, Mycobacterium tuberculosis and others
Gene homologs encoding curli were recently determined also in four phyla: Bacteroidetes, Proteobacteria, Firmicutes, and Thermodesulfobacteria
changes in the gut microbiota induced by antibiotics alter neuroinflammation and amyloid deposition in a mouse model of AD
Our data suggest that amyloid proteins in the microbiota are involved in the origination and maintenance of neurodegenerative disease.
exposure to bacteria producing a functional extracellular amyloid protein enhances aggregation of AS in brain neurons in aged rats and in muscle cells in nematodes
AS aggregates seed aggregation of tau
involvement of the vagus nerve in PD
microgliosis, astrogliosis and enhanced expression of IL-6, TLR2 and TNF in the brain following curli exposure suggest the occurrence of an enhanced local sterile inflammatory response to AS in the brain.
the immune system in both AD and PD have now been extensively established
TLR2 activation through exposure to bacterial amyloid is pathogenic
Gut bacteria may play crucial role in systemic inflammation that leads to Alzheimer's and Parkinson's disease. These amyloid production bacteria trigger systemic inflammation that leads to microglia activation and amyloid in the brain. More establishment of the gut-brain connection.