By Dale Bredesen, M.D., Chief Science Officer for Apollo Health

Two roads diverged in a wood, and I—
I took the one less traveled by,
And that has made all the difference.
— from The Road Not Taken, Robert Frost, 1915

A neurologist — a well-known and well-respected one, at that — runs a dementia clinic, and one of our ReCODE participants visited the clinic, both before and after some time on the protocol. She described the gloom that hung over the clinic and the hopelessness that permeated the waiting room and its occupants. Fortunately, she has done well, with sustained improvement on the ReCODE Protocol, and when she saw the neurologist in follow-up, he was surprised at how positive her outcome had been, asking her what she had done.

There are hundreds of such dementia clinics, and virtually all follow the current standard of care: checking a few labs (like TSH and vitamin B12), getting a standard MRI, and treating with a drug — typically donepezil or memantine — telling the family to expect only decline.

Sadly, considering the present standard research efforts, the care model is unlikely to change: research seeks “the cause” of Alzheimer’s — amyloid or tau or misfolded proteins or free radicals or prions or Herpes or metals or any of many other theories, none of which has led to effective treatment — and develops drug candidates that address these various unproven theories. Over 40 billion dollars have now been spent on developing these failed pharmaceutical candidates.

Recently, a “historic breakthrough” was claimed (by the company that plans to profit from it), lecanemab. It does not improve cognition, nor does it stabilize Alzheimer’s, but in one unpublished trial, it was claimed to slow decline by 27%. Can you imagine if Elon Musk reported that all of the SpaceX rockets exploded, leaving no survivors, but he had a “breakthrough” that delayed the inevitable astronauts’ demise by 27%? Would that really be a “historic breakthrough”?

My laboratory colleagues and I set out, in 1989, to study the molecular basis for neurodegeneration, in the hope that an understanding would point us toward the first effective treatment for Alzheimer’s and related diseases. We ended up far, far from where we thought we would — with a view of Alzheimer’s as a network insufficiency instead of a simple, one-cause disease, with contributions from dozens of mechanisms such as leaky gut and insulin resistance and biotoxins, among many others, with the need to identify these various potential contributors, and with the first protocol that has reversed cognitive decline in patients with Alzheimer’s.

We ended up very much on the road less traveled — not in the development of simple drugs but in personalized, precision medicine protocols, which address the underlying mechanisms of Alzheimer’s and have achieved much better results. There is still so much more to do — how can we achieve success for every person? How can we treat very late-stage patients more successfully? How can we adapt the approach to each of the major neurodegenerative conditions (and we do have promising initial data in this area)? How can we convince everyone, including the children of every patient, to begin active prevention or early-stage reversal, so that we can truly make Alzheimer’s optional?

Even though there is indeed much more work that must be done, our results show us that we are on the right track. Despite criticism from those stuck with the outdated, over-simplified model of Alzheimer’s, from foundations to experts to companies, our results have outstripped those of any of our critics. We are indeed pursuing an untraveled path, but we hope that many others will make the same choice, because there are millions in need.

Two roads diverged in an Alzheimer’s wood, and I took the one less traveled by. And it has made all the difference.

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