How to Help Prevent and Treat Alzheimer’s Disease

Editor’s Note: This article is a reprint. It was originally published July 2, 2023.

In this video, I interview repeat guest Dr. Dale Bredesen, a neurologist specializing in the treatment of Alzheimer’s. In 2014, he published a paper¹ demonstrating the power of lifestyle choices for the prevention and treatment of this tragic condition. By leveraging 36 healthy lifestyle parameters, he was able to reverse Alzheimer’s in 9 out of 10 patients.

Randomized Trial Launch

For starters, his team has published another proof-of-concept paper and are now launching a randomized, controlled trial at six sites: Hollywood, Florida; Nashville, Tennessee; Cleveland, Ohio; and Sacramento, Oakland and San Francisco in California.

Biological aging, brain aging and epigenetics will be assessed in this trial, using newer blood tests that weren’t available even a few years ago, including phospho-tau 181, phospho-tau 217, A-beta 42 to 40 ratio, glial fibrillary acidic protein (GFAP) and neurofilament light polypeptide (NF-L).

“A couple of these are not commercially available yet, so we’re doing these as research, but they will all become commercially available,” Bredesen says. “Currently, phospho-tau 181 is commercially available and so is the A-beta 42 to 40 ratio. So now, for the first time, you can get an idea, without necessarily having a PET scan, where you stand.

More importantly, you can follow it as you improve. Prevention is key, but also reversing cognitive decline, which we were the first to do … We’ve seen it again and again, when you’re doing the right things, when you’re attacking the important drivers of the process, you see [reversal].”

Valuable Tests

The GFAP test, while nonspecific, can be a valuable tool. This test basically looks at brain changes associated with astrocytosis. Astrocytes respond when there’s a problem in the brain, so it can give you a heads-up that something is afoot up to 10 years before symptoms become apparent. “The good news is if it’s normal, you’re in pretty good shape. So you want to know that going forward,” he says.

The phospho-tau 181 and phospho-tau 217 are specific tests for Alzheimer’s changes related to the death of neurons. Genetic testing is also important to ascertain how many copies of the APOE ε4 gene you might have. “That’s a critical piece,” Bredesen says. “Everybody should know their APOE status.” Hormone testing and testing for toxins, including mycotoxins and heavy metals, are also important.

Where There’s Smoke There’s Fire

According to conventional thought, elevated tau and beta-amyloid are causative factors in Alzheimer’s, but Bredesen’s research suggests otherwise. He explains:

“This is a little bit like saying, ‘There’s some smoke there. If we just blow away the smoke, then the house is not going to burn down.’ It makes no sense. The key thing to know is that [tau and beta-amyloid] are responses and mediators. You’ve talked a lot about mitochondrial function, which is absolutely critical in this disease, but we know of many upstream contributors, and that’s another update.

People have not known what’s causing this disease, and it’s often said there’s nothing that prevents, reverses or delays it. Nothing could be further from the truth. We know there are many contributors, [including] anything that damages mitochondria [and] different infections.

What we now see from the research is that Alzheimer’s disease fundamentally is a network insufficiency. You have this beautiful network of about 500 trillion synapses and as you get exposed to inflammation, infections in your mouth, insulin resistance, leaky gut, not enough blood flow, reduced oxygenation, reduced mitochondrial function, any of these things, that network is no longer sufficiently supported.

And, no surprise, it pulls back and that’s why you see the tau. They are part of the mediators of making this effect enhanced. They amplify the problem. Dr. Lee Hood and Dr. Nathan Price have just published a wonderful book called ‘The Age of Scientific Wellness,’ and as they point out, amyloid is an excellent biomarker but a terrible therapeutic target, and that’s exactly what’s coming out of the data.

Unfortunately, Lecanemab was just recommended by the panel for FDA approval. It slowed the decline. But here’s the thing they didn’t say, which they should have said, what are the things that performed better? Lecanemab doesn’t make you better, it doesn’t keep you the same, it slows the decline by 27%. That’s it.

So what worked better in their trials? No. 1, ketones alone worked better than this drug. No. 2, extra virgin olive oil alone in a trial worked better than this drug. No. 3, combined metabolic activators — carnitine, nicotinamide, riboside, things like that. Again, supporting energetics. This is about energetics and inflammation. Those are the two big players.

And then of course, the protocol we developed worked the best of anything. We’ve got people now who have sustained their improvement for more than 10 years. So, it’s sad that this drug has been recommended for approval.”

Two Key Causative Factors That Must Be Addressed

According to Bredesen, supporting energy and reducing inflammation in the brain are the two most important factors to prevent and treat Alzheimer’s. Basics that all of Bredesen’s patients implement include: