Can we prevent Alzheimer's? Scientists say new tests and treatments are "a game changer"

I often feel that as aggressive longevity and health extension people, dementia/AD (and cancer) are less under our control than metabolic, cardiovascular and other vital organ related diseases and hence found some of the perspectives in this new Newsweek piece interesting


When Aisen started, Alzheimer’s disease was thought to begin with the onset of observable cognitive and functional decline and, after progressing for seven years or so, result in death. But the onset of early dementia, we now know, is in fact just the final phase in a far longer progression that takes place over roughly 25 years. It begins with the accumulation of amyloid-beta at least 18 years before any behavioral changes are detectable to most future patients or their loved ones.

“For all of history, people have been afflicted by senility and dementia, and for thousands of years, you couldn’t do anything about it,” says Bateman. “Even in recent history, you could only diagnose people after they died. Now a single blood sample can with 95 percent accuracy identify Alzheimer’s. And in just six to 18 months, we can remove plaques from the brain that have built up over 20 years. We can for the first time change the course of how fast the disease progresses. To me, it’s just absolutely incredible. It’s really profound.”


Reiman, in fact, believes these side effects might be less of an issue for those in an earlier phase of the disease. In the late stages, he says, “you’re having to pull amyloid plaque out of the brain, but also off of blood vessels, which is the main reason for the side effects,” such as bleeding and swelling, he says. In the brains of those who are at earlier stages of the disease, the plaques “haven’t been there as long. So, they’re less adherent, and you may have fewer side effects as well.”

Interesting perspectives here on how very early action via the new FDA drug(s) (and others in the pipeline) could
(a) perhaps have a big impact on preventing AD and
(b) perhaps also have a much better safety profile in those early stages such that early intervention might make sense

The next 5-10 years may be quite exciting and interesting here:

In the hopes of further arresting this systemic collapse, Aisen is co-leading the AHEAD trial, which is in the midst of recruiting “presymptomatic” patients to participate in a four-year study of lecanemab. The new cohort will consist entirely of people who are, for the most part, cognitively and functionally asymptomatic but have abnormal levels of amyloid in their brains. The idea is to capture people in years one through 10 of the progression. A later phase of the trial, he says, will target a cohort who is “even closer to year one.”

At the same time, the TRAILBLAZER study, co-led by Banner Institute’s Reiman, is taking a similar approach, but using donanemab, the new drug from Eli Lilly that is expected soon to win FDA approval, to target those in earlier stages of the disease.

It will take five years before AHEAD yields results, estimates Aisen, and 10 years before we have a real handle on how to prevent the disease. Reiman is slightly more optimistic but agrees many more steps are needed.

Still, both see a bright future ahead.

“Lecanemab is a real landmark. Having a fully approved drug [that] slows the disease is significant. But we’ve got to move on and increase the benefit,” Aisen says. “I’m very optimistic. We’re just going to build on this success. Things will get better and better until the entire population is routinely screened for risk and the risk is fixed before the disease starts.”

  1. More support for the thesis above that early treatment is more effective

  2. (home) injectable might as good or better than more cumbersome infusions; might have (non statically) higher risk AND more effect, but as discussed above these risks may be massively lower in early prevention vs later in the course:

Analysis of Lilly and Eisai’s Alzheimer’s trials suggests early treatment has greater benefit – Endpoints News

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Some researchers believe infections are a primary cause. Bacteria, yeast, viral. The article below reports on a new study linking candida to Alzheimer’s. Another review below discusses the possibility of bacterial infection being a cause. Doxycycline is an antibiotic that has the ability to both penetrate bacterial biofilms and cross the BBB. It has about a 24% penetration rate (100 mg x 4 = 400 mg daily). Fluconazole is reputed to be the safest antifungal medication, and also has the ability to cross the BBB. Doxycycline significantly potentiates the effects of fluconazole against candida, which may make it an effective combo.

Nitazoxanide has broad antiviral activity, also effective against a range of parasites and some bacteria. It is a benign medication with a good safety profile. It can cross the BBB, and has been shown to improve symptoms in AD model mice. It also promoted clearance of Aβ plaque. It also has mitochondrial uncoupling and autophagy enhancing properties. It also prevented atherosclerosis in mice fed a Western diet in a study. A possible antiaging compound. It also has significant anticancer activity. And there is preliminary evidence in animals that it may be an effective cholesterol lowering medication.


Broad-spectrum antiviral agents (BSAAs) and viruses they inhibit

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Thanks for this synthesis @Vlasko

Any sense of optimal protocols - how long treatments and how often to come back and dose?

I’m especially concerned about impact on our microbiomes - what are your thoughts on that? Any ways we can minimize the impact while still getting the positive effects if the antibiotics?

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You are aware that doxcycline is available in an injectional form for IV or IM. Avoiding the intestine track.

You can measure doxcycline levels in blood, Quest is one lab that can preforms this test.

In my view, FWIW people create too much BS about doxcycline. I have been taking 100mg every 8 hours since September 25th, 2023 without any issues.

As some members of this forum do not care for my reply on this subject.

Shamelessly Plagiarism

"Those that say in can not be done take a backseat to the people doing it”

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Thanks for this. Does that mean that there is no systemic effect back onto the gut microbiome?

Do you target anything specific level?

Look up the package insert for the injection version.

The test by Quest is test code 90493, review the information:

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What are people’s thoughts - could be huge? Eventually we all get apoe2…?

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