New research indicates that an experimental treatment might postpone Alzheimer’s symptoms in individuals genetically predisposed to develop the disease in their 40s or 50s. However, this study, which is a scientific breakthrough, is facing delays due to funding issues within the Trump administration. The findings were released on Wednesday, and participants in the study are concerned that political interference might hinder their access to what they see as a critical treatment.
Jake Heinrichs, a New Yorker, has been part of this study for over a decade, remaining symptom-free despite inheriting a gene associated with Alzheimer’s that proved fatal for his father and brother around the same stage of life. Heinrichs and his wife, Rachel Chavkin, are worried about the consequences if funding constraints halt his treatment, with Chavkin stating, “This trial is life.” Currently, two U.S.-available drugs can slightly slow the progression of early-stage Alzheimer’s by removing amyloid, a characteristic sticky substance in the brain. Previously, experts had not seen signs that early removal of amyloid, years before any symptoms, could potentially delay the disease’s onset.
The study, led by Washington University in St. Louis, involves families possessing rare genetic mutations, resulting in the same symptoms at similar ages as their relatives, thus offering researchers a basis to evaluate treatment effectiveness. The recent findings focus on a group of 22 participants who have received amyloid-clearing drugs for an average of eight years, which reduced their risk of symptoms by half, as reported in Lancet Neurology.
Despite the limited size of the study, experts like Northwestern University’s neuroscientist David Gate consider it crucial. The participants have now transitioned to Leqembi, a U.S.-approved IV treatment, to uncover how extensive the protection might be. Dr. Randall Bateman, directing the Dominantly Inherited Alzheimer’s Network, aims to understand if ongoing treatment can indefinitely prevent Alzheimer’s symptoms.
However, as Bateman raises funds to advance the research while awaiting National Institutes of Health (NIH) support, his grant is stalled due to required funding reviews being canceled, highlighting a broader issue with NIH funding amid restrictions and commotion.
There is also concern that NIH might deprioritize amyloid research, following comments from Dr. Jay Bhattacharya, the agency’s director nominee, emphasizing the need for a broadened range of hypotheses given previous setbacks in Alzheimer’s research. Alzheimer’s disease, impacting nearly 7 million Americans mostly in later life, is not well understood, but changes in the brain occur silently at least two decades before symptoms surface, with amyloid believed to play a significant role.
Currently, researchers are investigating alternative factors like inflammation and brain immune cells, along with tau-fighting drugs, as part of the effort to understand Alzheimer’s better. From 2013 to last fall, NIH’s funding strategy evolved, reducing the proportion of trials focused on amyloid amid growing research on other potential causes.
Northwestern’s Gate, still affirming the significance of amyloid, recently explored how immune cells known as microglia could eliminate plaques and aid brain recovery, offering insights for improving therapies. Still, for those with genes predicting Alzheimer’s, understanding whether blocking amyloid can delay symptoms is crucial and needs NIH funding to proceed.
June Ward, another study participant from Asheville, North Carolina, who is healthy at 64, is two years past her mother’s age of Alzheimer’s onset and is encouraged by the possibility that she might avoid the disease. Similarly, Heinrichs hopes his toddler son won’t endure the sorrow linked to Alzheimer’s, urging for NIH to stay unbiased and continue supporting vital research.
