We told you over a decade ago it was gastrointestinal.
See the Fucking Vortex.
Injecting animals with LPS reduces Orexin production, just like an infection.
Multiple teams have been researching Porphyromonas gingivalis, the main bacterium involved in gum disease, which is a known risk factor for Alzheimer’s. So far, teams have found that P. gingivalis invades and inflames brain regions affected by Alzheimer’s; that gum infections can worsen symptoms in mice genetically engineered to have Alzheimer’s; and that it can cause Alzheimer’s-like brain inflammation, neural damage and amyloid plaques in healthy mice.
“When science converges from multiple independent laboratories like this, it is very compelling,” says Casey Lynch of Cortexyme, a pharmaceutical firm in San Francisco.
Now researchers from Cortexyme and several universities have reported finding the two toxic enzymes that P. gingivalis uses to feed on human tissue in 99 and 96 per cent of 54 human Alzheimer’s brain samples taken from the hippocampus – a brain area important for memory (Science Advances, doi.org/gftvdt). These protein-degrading enzymes are called gingipains, and they were found in higher levels in brain tissue that also had more tau fragments and thus more cognitive decline.
The team also found genetic material from P. gingivalis in the cerebral cortex – a region involved in conceptual thinking – in all three Alzheimer’s brains they looked for it in.
“This is the first report showing P. gingivalis DNA in human brains, and the associated gingipains co-localising with plaques,” says Sim Singhrao at the University of Central Lancashire, UK, who wasn’t involved in the study. Her team has previously found that P. gingivalis actively invades the brains of mice with gum infections.