A pre-print study posted in May 2021 shows positive results in a clinical trial with the goal of reversing early Alzheimer’s disease.
This is big!
An attitude of acceptance that Alzheimer’s is a non-reversible fate prevails in medical practices, and a positive clinical trial showing marked improvement in many participants is wonderful to see.
The clinical trial used Dr. Dale Bredesen’s protocols for Alzheimer’s prevention, much of which he has outlined in his book, The End of Alzheimer’s.
Why am I writing about a pre-print? This study seems to be of very high quality and backed by a lot of other research. It comes together showing a personalized approach to Alzheimer’s prevention is the right approach. I’ll update this article whenever the preprint is published in a major scientific journal.
Clinical trial to reverse Alzheimer’s
Let’s take a look at the clinical trial:
The study involved 25 patients (ages 50-76) with either Alzheimer’s disease or mild cognitive impairment. The Montreal Cognitive Assessment (MoCA) was used to quantify the degree of cognitive impairment.
The researchers evaluated the participants for “markers of inflammation, chronic infection, dysbiosis, insulin resistance, protein glycation, vascular disease, nocturnal hypoxemia, hormone insufficiency or dysregulation, nutrient deficiency, toxin or toxicant exposure (metals, organic toxicants, and biotoxins), genetic predisposition to cognitive decline, and other biochemical parameters associated with cognitive decline.“
Researchers then used this information to create a personalized protocol for each patient.
The study participants were then followed for 9-months, with cognition tests every three months.
Genetically, the participants covered a range of APOE types (E2/E3, E3/E3, E3/E4, and E4/E4). If you have 23andMe genetic data, you can check your APOE type here, if you want to know.
Before we get into the results, a couple of things stand out about the trial…
First, it is awesome to see a study using so many different parameters and personalized targeted interventions. But, it is important to note that the participants were younger than many Alzheimer’s patients. Additionally, the study participants were almost all college graduates, with almost half of the cohort having a graduate degree. Both of these factors make it more likely to have a positive outcome than a general population group. This was a proof-of-concept clinical trial, so I would assume that the researchers chose the participants carefully.
The protocol for all participants included:
- All participants were encouraged to exercise (aerobics and strength training) for 45 minutes a day for 6 days a week.
- Sleep hygiene was encouraged, and sleep apnea was treated.
- Everyone ate a diet that included a lot of organic high-fiber vegetables (raw and cooked) and pastured eggs and meat. The diet was ‘mildly ketogenic’ and avoided processed foods, gluten, and dairy.
- The participants used biofeedback, heart-rate variability training (HeartMath), and brain training.
Individual protocols included:
- Hormone replacement when needed.
- Thyroid supplement for participants with less than optimal thyroid function.
- Vitamin D, omega 3, B-vitamins, CoQ10, and minerals were supplemented for people who had suboptimal levels.
- Gut healing protocols for people with leaky gut, inflammation, infection, or impaired digestion.
- Anti-inflammatory herbs for people with systemic inflammation. Low-dose naltrexone was prescribed for some.
- Anti-virals were prescribed for Herpes simplex and an herbal protocol given for active Epstein-Barr virus. For tick-borne infections, herbal antimicrobials and immune system support were given.
- Detoxification protocols were used for people with heavy metals, biotoxins, and organic pollutants (e.g. phthalates, organophosphates). This was done with binding agents, sauna, herbs, and restricting mercury-containing fish.
Results of the intervention:
A caregiver questionnaire showed that 84% of patients improved (mild to marked improvements). This is a great result since caregivers are likely to have a keen eye for either improvements or declines.
What about the Montreal Cognitive Assessment? 76% of participants improved their scores, 12% declined in scoring, and 12% remained the same.
You may be thinking, “Why didn’t everyone improve?” Good question, but important here is that most people without intervention would have shown a decline in cognitive scores over 9 months. So 76% improving scores and 12% remaining the same is pretty impressive.
The results are not broken out by APOE genotype, though, which is something that I would be interested in seeing. I would be most interested in knowing if any of the E4/E4 carriers were able to improve. But in the discussion section of the study, the researchers report that “both groups—the ApoE4+ group and the ApoE4- group—showed statistically significant improvements in MoCA and NCI (Neurocognitive Index) ”
Research on Alzheimer’s disease shows that there are likely many different contributing factors to the pathology. A single intervention – drug, lifestyle change, etc – is unlikely to be effective. Instead, this proof-of-concept clinical trial points to the efficacy (and common sense) of using multiple interventions that target many different factors that contribute to the risk for Alzheimer’s disease.
Want more information? Check out Apollo Health. This healthcare group is implementing Dr. Bredesen’s protocol with testing, nutritional plans, supplements, cognitive training, medical practitioners, and health coaches.
The time to prevent Alzheimer’s is in the decades before symptoms begin.
Interested in how your genetic variants could play into the different risk factors for Alzheimer’s? Check out the following Genetic Lifehacks articles:
- Melatonin receptors and Alzheimer’s disease risk
- TNF-alpha: Inflammation and your genes
- Serotonin 2A receptor variants: psychedelics, brain aging, and Alzheimer’s disease
- TREM2 and Alzheimer’s Disease risk
- Lithium orotate and Alzheimer’s
- A Klotho gene variant reduces Alzheimer’s risk in APOE E4 carriers
- Genetic mutations that protect against Alzheimer’s disease