The journey to find an effective treatment for Alzheimer’s disease has been long and fraught with more setbacks than successes.
Recently, the withdrawal of aducanumab, a drug approved for early-stage Alzheimer’s, and the FDA’s hesitation on approving a similar medication have spotlighted the complexities of fighting this disease.
Insights from Dr. Mike Greicius, a neurologist at Stanford Medicine, offer a deep dive into the challenges and misconceptions surrounding the current approach to Alzheimer’s treatments.
Alzheimer’s disease affects over 6 million people in the U.S., with numbers only expected to rise. Traditional treatments have barely scratched the surface, offering minimal relief by targeting symptoms rather than the root causes.
Aducanumab, along with its counterparts lecanemab and donanemab, represents a modern class of treatments aiming at a presumed cause of Alzheimer’s: amyloid plaque build-up in the brain. While these drugs excel at removing plaque, their impact on improving patient well-being is minimal.
The premise of attacking amyloid plaque stems from its association with Alzheimer’s cognitive decline. However, Greicius and his colleagues argue that plaque might not be the best marker of the disease’s progression.
Many people accumulate plaque without showing significant cognitive deterioration, suggesting that amyloid deposits might not be the culprit they were once thought to be.
Further complicating the issue is the focus on amyloid plaque to the exclusion of other biomarkers, like neurofibrillary tangles composed of tau protein, which correlate more closely with cognitive decline.
This oversight has steered research and development efforts in a direction that may not address the underlying mechanisms of Alzheimer’s disease effectively.
The clinical trials for these plaque-targeting drugs have shown statistically significant results, yet the real-world impact on cognition is negligible.
This discrepancy raises questions about the trials’ design and the placebo effect, exacerbated by side effects such as brain swelling and bleeding, which could inadvertently reveal to participants whether they were receiving the actual treatment or a placebo.
Additionally, genetic factors like the APOE4 variant, associated with a higher risk of Alzheimer’s and increased susceptibility to the drugs’ side effects, further complicate trial outcomes.
Adjusting trial data to account for these side effects might inadvertently skew results, making the drugs appear more effective than they are.
Greicius’s critique underscores a critical need for a shift in Alzheimer’s research. While reducing amyloid plaque does not seem to significantly improve patient outcomes, exploring other avenues—such as targeting tau tangles or understanding the genetic underpinnings of early-onset Alzheimer’s—may provide new directions for developing more effective treatments.
The FDA’s cautious stance on new amyloid-targeting drugs reflects growing skepticism within the scientific community about the current approach to Alzheimer’s treatment.
As researchers like Greicius call for a broader perspective on the disease’s pathology, the path forward requires not just innovative treatments but a deeper understanding of Alzheimer’s complex nature.
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The research findings can be found in the Journal of Alzheimer’s Disease.
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