#6

Yes, a little after turning 78. Her STM had been a famial point of concern for a few years before, mild but present. Her sister died at 75 after 3.5 years of really heartbreaking A-D progression.

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#7

This conclusion was based from one mice study I believe. On other hand there many more studies purporting improvement in cognition in mice.

Matt Kaeberlein says it best here:

It is possible that rapamycin might only be effective at delaying AD if treatment is started before the disease has progressed to the point of clinical diagnosis. However, at least a subset of preclinical studies reported positive effects of rapamycin in mouse models even after substantial AD-like cognitive deficits and histopathology were present (17, 20). These observations, combined with the ability of rapamycin to improve function in other tissues, most notably the cardiac and immune systems (29, 32, 38–41), raise the possibility that cognitive function could be improved in patients with early- or moderate-stage AD even after substantial cognitive decline. Optimally, we would recommend clinical trials for rapamycin efficacy both in patients with MCI who are likely to progress to a diagnosis of AD and in patients recently diagnosed with AD.

In fact the current human trial did jus that, pick candidates with MCI and early dementia for the rapamycin study.

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#8

Hello Deborah,
Have you checked of your ApoE4 allele status? People with one or both are at an increased risk for AD.

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#9

Thanks for your responses. The paper that talks about the potential harms of RAPA after onset of AD is: “Rapamycin and Alzheimers Disease: A Double-Edged Sword?” published 5/22/2019 in Autophagy.

If you read it I would appreciate your assessment –

I am encouraged by your inputs that Rapa has actually helped after onset of disease.

No, I do not have the APOE4 phenotype – I am APOE3. My main concern is actually that I will live long but be demented, as my mother (age 97 today) is now, even though my health and behaviors are very different from hers.

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#10

@Deborah_Hall I took a look at the literature. Seems like you won’t get a clear answer because there just isn’t one yet. Human studies ongoing.

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#11

Yes. See our thread here: Rapamycin and Alzheimer disease: a double-edged sword?

Other discussion threads related to Alzheimer’s and rapamycin:

  1. Rapamycin and Alzheimer Disease: a Hypothesis for the Effective use of Rapamycin

  2. Fighting Alzheimer’s with Increased Autophagy via Rapamycin + Trehalose

  3. UT Health San Antonio gains $2M to study rapamycin for Alzheimer’s

  4. New Study: Rapamycin protects against Alzheimers in Mouse Model

  5. Intranasal Rapamycin Lessens Alzheimer-like Cognitive Decline in a Mouse Model of Down Syndrome

  6. Rapamycin increases Alzheimer's-associated plaques in mice, study finds

  7. A drug cocktail of rapamycin, acarbose, and phenylbutyrate enhances resilience to features of early-stage Alzheimer's disease in aging mice

  8. Rapamycin restores peripheral blood flow in aged mice and in mouse models of atherosclerosis and Alzheimer's

  9. Rapamycin and AD

  10. Mitophagy Activation by Rapamycin Enhances Mitochondrial Function and Cognition (New Study)

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#12

I would try this https://pendulumlife.com/products/pendulum-glucose-control-2-og

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#13

Definitely want to get the blood glucose under control: Diabetes, air pollution and alcohol consumption could be the biggest risk factors for dementia

And, it seems research may support the idea that you want to get the blood glucose well under control before you start rapamycin: People With These Health Conditions Should Not Take Rapamycin?

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#14

Indeed - Type 3 Diabetes - is essentially what many of us think is a substantial cause of late dementia. This is a different situation, potentially, than early dementia, which is multi-factorial, including ApoE4 positivity.
Insulin resistance and lack of proper utilization of glucose in the brain is likely a cause of some of the pathological changes in the brain with late Alzheimer’s Dementia.
I suspect this is why, diabetic drugs are having such strong signals as medications to decrease cognitive decline and probably also Parkinson’s Disease.
Other factors including solid use of the brain, include optimizing Omega 3 index, tight blood glucose/pressure control, management of stress/sleep/social connections, adequate whole food plant based diet for photochemicals/gut health, and adequate exercise.
It’s a big package to implement - and rapamycin is certainly part of the mix here - but it’s only part of a bigger lifestyle to obtain better health outcomes.
Those of us in the longevity medicine space advise our patients that only 15% of health outcome is genetics — 85% is life choices. This is a double edged sword, as so many people look at their elders and think that their parents living to 95 is relevant. Their exposures, diet and activity are often dramatically different. On the other side, people who have parents with huge comorbidities and death earlier in life - should be encouraged, in general - if their parents made very poor lifestyle choices (smoking, lack of proper management of medical conditions, sedentary, obese, etc) - that it is not going to be their health outcome if they manage their conditions and co-morbidities.

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#15

Are you aware of any independent data supporting this product?

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#16

Both from experience and from research available at PubMed, I strongly (that really should be all caps) recommend looking into taurine. In animals, it prevents or halts neurodegenerative diseases including Alzheimer’s and Parkinson’s. Last I looked, there were promising results in early human trials.

Experience: Two years ago, when I was 73, I began taking 2000 mg a day of taurine. Two days later, waking up was like waking up to a whole new reality. For some time, I had been forced to enter the first three digits of a six-digit security code and then look at the second half again. That problem was gone. Two weeks after that, I needed a 15-digit part number, read it twice, and still remembered it weeks later.

I also recovered cognitive abilities I had not been aware of losing. For some time, when faced with a minor difficulty in some minor chore, I had simply plodded on until it was done. Suddenly, I was automatically reaching for something nearby that would solve the problem–a paper, a bit of string, a spreading knife–whatever was handy and none of them used for their original purpose.

Owing to that research on lifespan a year or so ago, I now take 5500 mg per day at 160 lb weight. That is how the standard animal-to-human conversion came out. Adjust as required.

Strongly recommended.

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#17

Thank you for this. Have been taking a low dose of Taurine but will increase and start my husband on it as well.

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#18

Below is a new review on composition of drinking water and incidence of cognitive decline in the elderly. Alkaline water and silica may be protective. Silica may also reduce absorption of aluminum. Perhaps avoid acidic beverages like soda in favor of alkaline teas.

Both alkaline water and organic silicon may have general anti-aging benefits per animal studies as well. I take an orthosilicic acid supplement in my daily collagen drink. Promotes collagen synthesis, improves nail quality.

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#19

No independent data yet, I don’t think. But some confirmation from people (anecdotal)… discussed here: Akkermansia mucciniphila improves healthspan and lifespan in old female mice - #3 by Pestodude

#20

I work with Alzheimer’s patients, am one of the authors on the Precision Medicine Trial published 8/22. The biggest contributors to AD for ApoE3/3 women are insulin resistance and failure to replace hormones (bio-identically) @ menopause. Toxins also play a role, especially mold and Lyme. Lab Corp now has an even better test, ATN panel with measurements of amyloid beta, pTau, and Neuofilaments.

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#21

Hey there!

I had a very bad experience with the Quest test. The results came back “bad,” which completely freaked me out. I made massive lifestyle changes, including looking for clinical trials to join.

Fortunately, I found one, called the AHEAD trial, that gives you some sense of what their screening tests show (not always the case). After more extensive testing through them, they told me I did not qualify for their trial, which I interpret to mean that my results aren’t as bad as shown in the Quest test.

I had a discussion with the investigators about how their results could be so different from the Quest results and how it had upended my life, which ended with them saying, “That company is going to get sued.” My understanding now is that the test results don’t correlate well with actual progression to dementia. “Bad” test results don’t mean much in practical terms.

As an aside, the Quest doctor who went through my scary test results with me on the phone was absolutely worthless. First, he told me the results were the opposite of what they actually were because he was reading it wrong, and second, he answered every question with “You’ll need to talk to your doctor about that.”

But there is actually a better test that just became available that researchers seem to think is more predictive called the p-tau 217 test, which I’m thinking about getting (because all the lifestyle changes that might prevent or delay Alzheimer’s are freaking hard and time-consuming, so I don’t want to do them all if I don’t need to).

If you want good information about preventing Alzheimer’s, I recommend this forum for people who have the APOE e4 allele (which raises genetic risk): https://www.apoe4.info/

Dale Bredesen’s book “The End of Alzheimer’s Program” is also good. (He recommends many tests, but I found out after I took the Quest test that he doesn’t recommend that particular test.)

Good luck! I know that fear of watching close relatives go through Alzheimer’s and wanting to do everything you can to avoid it.

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#22

Thanks for the post - sorry to hear about the roller coaster. May I ask what battery of lifestyle changes you made?

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#23

Sure, none of them alone are that hard. It’s just doing all of it that becomes taxing.

  1. Following a strict “healthy” keto diet. This is mostly fish, vegetables, and berries with lots of high polyphenol (read “expensive”) olive oil.

  2. Doing aerobic exercise 5 times a week. I did a mix of HIIT and regular aerobics.

  3. Weight training every other day.

  4. Meditating every day.

  5. Walking every morning outside for ~30 minutes.

  6. Flossing twice a day.

  7. Making sure I move at least once an hour and don’t just sit at my desk for hours.

  8. Making sure I always get enough sleep. (This is one of the most important things and was hard to achieve, but easy to keep doing once I figured it out. We put blackout curtains in our bedroom, and I take melatonin plus a big dose of tryptophan (2g) right before bed.)

The following are all just ways to challenging the brain with new and different activities:

  1. Upping the time I spend learning Spanish.

  2. Playing the piano.

  3. Daily Brain HQ games. (These have some data behind them for AD prevention, but I hate them. They are hard, and they were the first thing I quit when I wasn’t so scared. “Games” is a misnomer! When I mention this to people, they often say something like “Oh, I do crossword puzzles.” It is nothing like that.)

  4. Actively trying to have more social interactions with people.

  5. Making sure I smell a lot of different scents every day. (This probably has the least evidence of being helpful of anything I did, but it’s also easy.)

I think these are the big things off the top of my head. They aren’t everything you could possibly do (some people do sauna, exercise while breathing oxygen, etc.), but they are what I felt I could do.

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#24

Very helpful. Thanks a bunch.

#25

I think your list is good, but it is certainly impractical for me to do many of the things you mention.
Unfortunately, genetics plays a big role. The number of things on your list that you must do probably depends on your genes.

“Early-Onset Alzheimer’s Disease
Caused by mutations in APP, PSEN1, PSEN2 genes
Autosomal dominant inheritance
Symptoms develop before age 65
Late-Onset Alzheimer’s Disease
APOE e4 allele is the strongest known genetic risk factor
Over 20 other genetic loci associated with small increases in risk
Heritability estimates around 60-80% for late-onset A”

3 Likes