DIAN-TU Trial: Another Failed Monotherapy for Alzheimer’s

by Amylee Amos PhD, RDN, IFMCPNews
DIAN-TU Trial

This past week, news broke that yet another massively anticipated Alzheimer’s drug trial has failed. The study, funded in part by pharma giants Eli Lilly and Roche, was called DIAN-TU (Dominantly Inherited Alzheimer Network Trial: An Opportunity to Prevent Dementia). The study was a Phase II/III randomized, double blind, placebo controlled, multi-center study- the gold standard of clinical trials. The trial looked into the efficacy of two drugs: Gantenerumab and Solanezumab in individuals who carry genetic variants of particularly high penetrance (PSEN1, PSEN2, APP). The drugs were designed to target amyloid, the protein known to cause sticky plaques in the brain’s of Alzheimer’s patients. Researchers of DIAN-TU hoped that by using participants who had not yet developed Alzheimer’s, they could prevent it by utilizing these drugs.

However, after monthly injections or infusions of these drugs over an average of 5 years, along with annual brain scans, cognitive testing, and blood draws, the results were in: the drugs did nothing to slow or stop the progression of Alzheimer’s disease. Another huge blow to the search for an answer to Alzheimer’s disease by big pharma.

With the incredible humanitarian, economical, and emotional burden of Alzheimer’s disease, it would be truly wonderful if researchers could find a single pill that could cure or prevent the disease. But the fact is, it’s looking more and more like that’s never going to happen. Alzheimer’s disease is too complex to be solved by a single monotherapy. There is no one thing that causes Alzheimer’s disease. There are many things, even within individual people- there are many contributors to Alzheimer’s disease and they all need to be addressed using a multi-therapy approach. Researchers seem to be stuck on the issue of amyloid plaques and as a result funnel billions of dollars and countless hours into research to stop the creation of amyloid or to clear it from the brain. Yet they fail to ask why the amyloid is accumulating in the first place. And in other ways this is an issue of all chronic diseases: a focus on the what, instead of a focus on the why.

Of course there is a genetic component, especially in these very rare, high penetrance genetic variants, such as those studied in this trial. But carrying the variant doesn’t guarantee a diagnosis of Alzhiemer’s disease, and that is especially true in the far more common genetic variant ApoE4. What will it take for the greater medical community to look beyond the outdated one pharmaceutical for one disease model of the 20th century and instead embrace the multi-therapy, with nutrition and lifestyle medicine for complex chronic illness model that the 21st century desperately needs? Perhaps it’s not so much that another drug trial has failed, but that the whole system of pharmaceutical monotherapies has failed. We know that the Bredesen Protocol works to reverse cognitive decline. It’s complex and it’s certainly not easy, but imagine how much we could learn and how many people could be helped if the money and effort dedicated to this outdated system was instead channeled toward a functional approach such as the Bredesen Protocol.

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