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All the other Alzheimer's researchers are not infectious-disease specialists, and have no reasonable prospect of becoming infectious-disease specialists. The overwhelming majority of Alzheimer's disease research funding still goes to them. They get veto power over most potential grants to infectious-disease groups, and publication by them in most journals.

Probably the single most effective way to enable progress on Alzheimer's research would be to discover something else they could all work on, and stop blocking infectious disease specialists' work.

Amyloid plaque accretion reminds me of cholesterol accretion, and there is a recent school of thought whereby:

- Heart disease is actually caused by metabolic syndrome (read: same cause as diabetes)

- Alzheimers is analogous to diabetes (some are calling it Type 3)

I'm not convinced of the above, but it's interesting.

I found both theories promising.

Your post reminded me of this pub: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3709085/

I find the more studies I read, the higher the stakes seem, because the theories I've read are highly contradictory yet their proponents seem very polarized and very sure of themselves. Some theories that have been prematurely accepted by some groups are going to be very, very wrong.

The easiest example of this sort of highly polarized dynamic is in the realm of diets.

> If this theory, which Moir outlines in a review article published in the December issue of the journal Alzheimer's & Dementia, proves true, it could mean researchers' current strategies to combat the disease — fighting the plaques — is misguided.

But it could still mean that preventing the plaque formation would stop the dementia, right?

No, if the plaques are symptoms of a disease, supressing them equals supressing infection symptoms (fever)- you basically feel better but actually prolong the disease and accelerate it somewhat.

>you basically feel better but actually prolong the disease and accelerate it somewhat.

That might be totally fine if the effects of the disease the plaques fight are not as bad as the disease they cause -- e.g. the "prolonged" disease is not as bad as Alzheimer.

But that's worth exploring, right? I'm sure many people would prefer a lucid but shorter life than a longer one that is highly impacted by dementia symptoms

I think the idea is that the plaques are symptoms and that we should invest in the root cause. Like developing antibiotics instead of fever reducers. They both have a role, and I know where I'd allocate my resources.

Afaik, the drugs that reduce plaques have failed to actually alleviate symptoms of the disease.

The emphasis on the plaques comes from the fact that Alzheimer’s is diagnosed by the presence of these plaques, while dementia is a symptom/presentation.

I guess it comes down to whether you believe that an infection disproportionately affects old people and causes dementia. It probably doesn’t, not for any good biological reason, but because it doesn’t sound like any progress has been made on the biomechanics of dementia.

Laypeople obviously don’t care about the plaques. They want the dementia to go away. You can make a mouse model that has a brain infection, and then potentially a model where that infection shows plaques, and then a molecule that gets rid of the infection. But it’s really hard to tell (in real life, not in science speak) if a mouse has dementia. That’s the limitation.

We’re so incredibly far away from drug interventions for dementia.

> I guess it comes down to whether you believe that an infection disproportionately affects old people and causes dementia.

What they're saying is that after many years of fighting the infection Alzheimer's starts to develop. Certainly people who are older have the potential to have more years of infection. This seems plausible.

>I guess it comes down to whether you believe that an infection disproportionately affects old people and causes dementia. It probably doesn’t, not for any good biological reason

How about older people not having the health required to fight the infection?

There is a clinical trial associated with the anti-gingipain treatment described in OPs study that is going into phase 2 this month. If the authors are correct, people are going to be getting this treatment for alzheimers this year.

given the catastrophic failure of every single plaque therapy ever tried over the last 30 years, i’m going with “certainly misguided”.