In Beating the Dementia Monster, we wrote that "young onset" or "familial" Alzheimer's disease is caused by three unusual genes, and these almost surely guarantee that you will develop the disease, perhaps as young as in your 30s. We also wrote in 2022 that the testing of the monoclonal antibody gantenerumab was discontinued by Roche because it appeared to be ineffective against familial or any form of Alzheimer's.
As with the other monoclonal antibodies (think Kisunla and Leqembi), the treatment is able to remove the plaques of amyloid beta from the brain. Since development of these plaques is part of how we define the disease, logic said that getting rid of them should slow or even stop development of the disease. We call this the amyloid hypothesis. But, in the case of gantenerumab, it didn't. And so Roche gave up on it.
But hold the presses! There's a new study finding that gantenerumab can actually cut the incidence of the development of familial Alzheimer's in half!
So what's different this time? Well, according to a study published in the April 2025 issue of The Lancet, the key is start early. Like, decades early. We know that the disease begins as much as 20 years before the first symptoms, so start the antibody treatment then.
How do you know that it's 20 years before you will develop memory loss and other symptoms of Alzheimer's? With "old onset" or "sporadic" Alzheimer's, that's a challenge. But, since familial Alzheimer's is so easily recognized in someone's DNA analysis, and since family member with one of the genes all tend to develop symptoms at about the same age, this becomes a fairly straightforward task.
The study by researchers largely associated with Washington University, St. Louis involved 73 people with one or more of the genes responsible for familial Alzheimer's. This genetic makeup all but guaranteed that they would develop Alzheimer’s disease symptoms in middle age. For a subgroup of 22 participants who had no cognitive problems at the start of the trial and who received the drug the longest (an average of eight years) the treatment lowered the risk of developing symptoms from essentially 100% to about 50%. Pretty amazing.
A couple of things though. This was over an eight-year period. If they continue the treatments, we still don't know if any of the participants will eventually develop memory loss or other symptoms of the disease. Also, monoclonal antibody treatments can lead to micro-hemorrhaging in the brain, and two study participants had to be removed because of this. So part of the treatment is administration of regular MRIs to watch for the development of brain abnormalities. And because work with gantenerumab had been discontinued, the study treatment was shifted from gantenerumab to Leqembi. Leqembi appeared on the scene late in the study, but has been shown to produce better results than gantenerumab.
So it may be that this discovery will only have value for people likely to develop familial Alzheimer's. We can't accurately predict those who will develop sporadic Alzheimer's (after age 65), so we won't know if or when to begin treatment. On the other hand, the ability to treat people who might develop the disease when they still have young families could be a real breakthrough.
I appreciate the comment from an unknown reader of this blog who brought this news to my attention.
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