When we think of Alzheimer’s Disease, we think of plaque that accumulates in the brain, and current conventional treatments focus on either reducing the buildup of amyloid plaque, or destroy the plaque. The ‘amyloid hypothesis’ has predominantly been what’s focused in the treatment of Alzheimer’s Disease.
In our previous post, we talked about β-Amyloid as an antimicrobial. Here we will develop that even more! There are some recent findings and literature where it’s not just a matter of plaque buildup, but what’s contained in the plaque. Researchers have found that bacteria have been found in the brains of people who have had Alzheimer’s for when they were alive. One of the bacteria found is P. gingivalis.
P. gingivalis is the main bacteria that is involved in poor dental hygiene and gum disease. This bacterium has been found to invade and inflame the brain in the areas correlating to Alzheimer’s [1].
How does P. gingivalis cause Alzheimer’s and dementia? It could potentially be a direct or indirect cause. P. gingivalis can directly damage the brain via inflammation, or indirectly by triggering the release of amyloid from the brain which is the brain’s protective mechanism, and can kill its own neurons over time.
But to what extent P. gingivalis can affect us, may depend on many other aspects too, especially our APOE status. Because APOE4 puts us at more risk of Alzheimer’s Disease, those with APOE4 may respond more intensely to the presence of P. gingivalis leading to faster accumulation of amyloid.
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https://www.newscientist.com/article/2191814-we-may-finally-know-what-causes-alzheimers-and-how-to-stop-it/?fbclid=IwAR0UJGi5cXfAfbTcbnFPnBTLcuaAf3iSPNFFu_OTbltO5SbeWakwbLV34hI