, the most common form of dementia, affects over six million people in the US alone. By 2050, the number of people aged over 65 with the neurodegenerative disease is anticipated to grow to more than 12 million.
Treatment options for the condition are limited. Just this week, Biogen鈥檚 aducanumab became the first new to be approved by the US in 20 years 鈥� and scientific opinion is divided over how beneficial the treatment will be for patients.
Over 100 prospective AD drugs have failed in trials over the past decade, and the few that have shown promise focus on slowing the progression of the disease, rather than tackling its underlying causes. Now, new research suggests that medicine could someday achieve what is currently impossible: reversing the effects of Alzheimer鈥檚.
A personalised approach
A trial using precision medicine to target the key drivers of Alzheimer鈥檚 has become the first to show improvement in patients living with the disease. The results, published in in May, showed that 21 of the 25 participants in the small, proof-of-concept study demonstrated improved cognition after treatment. The findings established that using personalised treatments to target a range of contributors to Alzheimer鈥檚 is effective enough to warrant a larger clinical trial.
Previous AD clinical trials have focused on a single treatment modality. The study鈥檚 co-lead author Dr Dale Bredesen, neurodegenerative disease expert and chief science officer at AD-focused Apollo Health, says treating Alzheimer鈥檚 with a single therapy is a 鈥渂lind approach鈥� that often fails to address the primary drivers behind an individual鈥檚 cognitive decline.
鈥淵ou’re not asking 鈥榳hy did the person get cognitive decline?鈥�,鈥� he says. 鈥淵ou’re just giving them a drug.鈥�
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By GlobalDataThe subtypes of Alzheimer鈥檚
In their pursuit of a personalised approach to Alzheimer鈥檚, the researchers behind the study identified the primary drivers of the disease, which can range from pathogens and toxins to vascular disease.
鈥淭here hadn’t been success with precision medicine for Alzheimer鈥檚 because people hadn’t really made deep dives into what is causing this in each person,鈥� Bredesen explains. 鈥淪o in our case, we looked at many different variables, we determined the contributors to cognitive decline for each person, and then we targeted those.
鈥淲e described subtypes of Alzheimer鈥檚 based on these various parameters back in 2015, and we’ve seen this in the trial as well,鈥� he says. 鈥淭he idea is, you have to flip the script instead of just treating everybody with a Procrustean approach.鈥�
Bredesen likens the team鈥檚 Alzheimer鈥檚 strategy to precision medicine in cancer, where the driving genetic mutations in an individual patient are identified and then targeted.
鈥淚 think that this model, understanding what Alzheimer鈥檚 actually is, is allowing us to see it in a much more accurate light than in the past,鈥� he says, 鈥渁nd is allowing us to have much better results than have ever been documented previously.鈥�
Challenging convention
The team鈥檚 hypothesis about the nature of Alzheimer鈥檚 has long been met with scepticism, Bredesen says. The researchers first proposed a four-arm trial exploring multiple potential therapies for Alzheimer鈥檚 back in 2011, but this was rejected on the grounds that the study involved too many variables.
鈥淧eople are not easily going to change their minds about these things; they don’t want to be told they’re wrong, I get that,鈥� Bredesen says. 鈥淎nd of course, also, because you spend your whole career with this idea that a drug is going to come someday.
鈥淭ypically, the experts who are far along in their careers will never believe it, no matter what we publish. So, it’s really the students of the experts that we’re interested in 鈥� they’re the ones who are a little more open-minded.
鈥淥ver time, they’ll be the ones that actually bring this into practice.鈥�
The researchers were eventually granted approval to explore their hypothesis in 2019. The study鈥檚 promising findings indicate that a broader, personalised approach to treatment has the potential not merely to slow the effects of dementia, but actually reverse them. Bredesen is optimistic that the research could mean life-changing treatments for dementia patients in the future.
鈥淔undamentally, it’s not one thing that’s causing [Alzheimer鈥檚],鈥� he says. 鈥淎nd therefore, we need to take a very different approach. We need to look deeply into this, analyse it, and then target those things.
鈥淲hen we do that, the results are really spectacular.鈥�
