A study conducted by researchers at the University of Cincinnati suggests that a decrease in the protein amyloid-beta in the brain, rather than an accumulation of this protein, may be behind cognitive decline in individuals with Alzheimer’s disease. The researchers found that individuals who were able to produce enough Aβ42, an important protein for brain health, to keep amyloid levels within a normal range did not develop Alzheimer’s disease, despite having amyloid plaques present in their brains. This study challenges the prevailing belief that amyloid plaques are the main cause of Alzheimer’s disease, suggesting that increasing levels of Aβ42 could offer cognitive benefits.
The study, published in the journal Brain, analyzed data from about 26,000 people enrolled in 24 randomized clinical trials for new monoclonal antibody treatments approved for treating Alzheimer’s disease. These treatments unintentionally increased levels of Aβ42 in the brain, which the researchers believed may be associated with slower cognitive impairment and clinical decline. The findings indicate that Alzheimer’s disease may be more of a process of losing Aβ42 rather than accumulating amyloid plaques, as previously thought.
Dr. Alberto Espay, the lead author of the study, stated that future medications for Alzheimer’s should aim at increasing Aβ42 directly, rather than indirectly through treatments such as monoclonal antibodies. Another expert, Dr. David Merrill, suggested that looking beyond amyloid and focusing on modifiable health factors that contribute to Alzheimer’s disease could provide insights into new treatment approaches. Addressing modifiable risk factors, such as exercise and managing chronic conditions like diabetes and hypertension, may help increase soluble Aβ42 levels while improving cognitive function over time.
Karen D. Sullivan, a board-certified neuropsychologist, highlighted the significance of the study’s findings in challenging the current understanding of Alzheimer’s disease and the role of amyloid plaques. She noted that the study’s results may spark discussions within the Alzheimer’s community and prompt a reevaluation of treatment approaches. Further research is needed to elucidate the mechanisms of modifiable risk factors known to decrease dementia risk and explore non-drug approaches that could provide similar benefits without potential side effects associated with existing treatments.
Overall, the study conducted by researchers at the University of Cincinnati provides new insights into the potential role of Aβ42 in Alzheimer’s disease and challenges the prevailing belief that amyloid plaques are the primary cause of cognitive decline. By focusing on increasing levels of Aβ42 directly, rather than targeting amyloid plaques, future medications may offer more effective treatment options for individuals with Alzheimer’s disease. Further research into modifiable risk factors and non-drug approaches could also lead to a better understanding of how to prevent or slow cognitive decline in individuals at risk for Alzheimer’s disease.
