I remember a study from a few years ago that showed a compelling link between gum disease and Alzheimer's. What happened to that hypothesis? Has it gained any more traction?
[1] is probably the study you're thinking of. There's also [2] regarding herpesviridae, among others.
In short, there are good reasons at this point to believe that amyloid-β's primary function is as antimicrobial peptide, and thus various infections may cause the seeding of amyloid-β deposits. These deposits may then persist for years beyond any useful benefit, especially if the brain's clearance mechanisms are impaired.
Note that, per [2]:
Importantly, in the antimicrobial protection model, neurodegeneration is not mediated by pathogen activities that directly kill neurons. Rather, Aβ innate immune pathways targeting pathogens mediate the AD [Alzheimer's Disease] neuropathogenesis that leads to widespread neurodegeneration. Thus, our model is consistent with the amyloid cascade hypothesis and overwhelming data showing the primacy of Aβ in AD pathology.
[1]. Dominy et al (2019). Porphyromonas gingivalis in Alzheimer’s disease brains: Evidence for disease causation and treatment with small-molecule inhibitors. https://doi.org/10.1126/sciadv.aau3333
[2]. Eimer et al (2018). Alzheimer’s Disease-Associated β-Amyloid Is Rapidly Seeded by Herpesviridae to Protect against Brain Infection. https://doi.org/10.1016/j.neuron.2018.06.030
Note that tooth decay and gum disease are strongly linked to sugar consumption, high sugar consumption causes diabetes, and Alzheimer has been linked with type 2 diabetes. I don't know how popular this hypothesis is these days, but that's a possible link.
While it may be considered andectoal, this fits with what i've seen in my family. In my mind and from what i've read it seems to be more of a combination of factors - diabetes, an APOE gene, toss in a little depression/loss of purpose/retirement/isolation, etc
I think it would be good to bring more attention to noticing when things start to slip, because as things progress there can be less openess to trying new things/focus on maintaining state.
In short, there are good reasons at this point to believe that amyloid-β's primary function is as antimicrobial peptide, and thus various infections may cause the seeding of amyloid-β deposits. These deposits may then persist for years beyond any useful benefit, especially if the brain's clearance mechanisms are impaired.
Note that, per [2]:
Importantly, in the antimicrobial protection model, neurodegeneration is not mediated by pathogen activities that directly kill neurons. Rather, Aβ innate immune pathways targeting pathogens mediate the AD [Alzheimer's Disease] neuropathogenesis that leads to widespread neurodegeneration. Thus, our model is consistent with the amyloid cascade hypothesis and overwhelming data showing the primacy of Aβ in AD pathology.
[1]. Dominy et al (2019). Porphyromonas gingivalis in Alzheimer’s disease brains: Evidence for disease causation and treatment with small-molecule inhibitors. https://doi.org/10.1126/sciadv.aau3333
[2]. Eimer et al (2018). Alzheimer’s Disease-Associated β-Amyloid Is Rapidly Seeded by Herpesviridae to Protect against Brain Infection. https://doi.org/10.1016/j.neuron.2018.06.030