A new study finds that increasing a specific protein in the brain may help slow the progression of Alzheimer’s disease.
A long-held theory is that Alzheimer’s occurs when a protein called amyloid-beta 42 (Aβ42) builds up into plaques in the brain, damaging nerve cells and leading to cognitive decline.
Researchers at the University of Cincinnati have challenged this notion, and instead suggest that the disease is caused by low levels of healthy, functioning Aβ42, according to a press release from U.C.
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They based this hypothesis on the fact that newly approved monoclonal antibody drugs — including lecanemab (Lecambi) and donanemab (Kisunla) — have had the unexpected consequence of increasing levels of the protein in the brain.
A new study finds that increasing a specific protein in the brain may help slow the progression of Alzheimer’s disease. (iStock)
“New Alzheimer’s treatments, designed to remove amyloid plaques, inadvertently increase Aβ42 levels, and this may explain their positive effects on cognition that are similar to or even better than amyloid reduction,” study lead author Alberto J. Espay, M.D., professor of neurology at the Gardner Family Center for Parkinson’s Disease and Movement Disorders at the University of California, told Fox News Digital via email.
“Higher levels of Aβ42 after treatment were associated with slower cognitive decline, indicating that restoring this protein to normal levels may be more beneficial for Alzheimer’s patients than removing amyloid.”
In the study, researchers reviewed data from nearly 26,000 Alzheimer’s patients who participated in 24 randomized clinical trials for newly approved antibody treatments.
They compared patients’ cognitive abilities before and after taking the new drugs, and found that increased amounts of Aβ42 were associated with “slower cognitive impairment and clinical decline.”
The findings were published Sept. 11 in the medical journal Brain.
Understanding amyloid
According to researchers, amyloid plaques aren’t necessarily a bad thing.
“The collective evidence, along with other studies, suggests that amyloid plaques are a normal reactive brain response to a number of stressors, some infectious, some toxic, some biological,” Espy told Fox News Digital.
A long-held theory is that Alzheimer’s occurs when a protein called amyloid-beta 42 (Aβ42) builds up into plaques in the brain, damaging nerve cells and leading to cognitive decline. (iStock)
“These are signs that the brain is dealing with stress appropriately.”
The researchers called the amyloid plaques “tombstones of Aβ42,” and said they may not have any harmful effects on the brain.
“Most researchers don’t believe that Alzheimer’s is driven by a single biological mechanism.”
“Amyloid plaques do not cause Alzheimer’s, but if the brain builds up too much of them while defending itself against infections, toxins or biological changes, it cannot produce enough Aβ42, causing levels to drop below a critical threshold,” he said.
“That’s when the symptoms of dementia emerge.”
The study calls into question the long-held idea that amyloid plaques directly cause Alzheimer’s and that removing them is part of the solution.
“Beta amyloid is certainly an important and major factor, but we also know that tau proteins, the immune system, the vascular system, metabolic health, the environment and others all play a role in the disease process,” the Alzheimer’s disease specialist said. (AP Photo/Evan Vucci, File)
“Increasing Aβ42 levels without removing the amyloid — which is pretty pointless, and may even be harmful — is worth testing as a future therapy,” Espey said.
Looking to the future, the UC research team plans to investigate therapies that could increase Aβ42 levels without directly targeting amyloid.
‘A very complex disease’
Ozama Ismail, PhD, director of scientific programs at the Washington, D.C.-based Alzheimer’s Association, was not involved in the UC study but commented on the findings.
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“Although this Aβ42-related hypothesis may prove to be a cause and catalyst for the development of Alzheimer’s, it is a very complex disease, and most researchers do not believe that Alzheimer’s is driven by a single biological mechanism,” he told Fox News Digital.
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“Beta amyloid is certainly an important and major factor, but we also know that tau proteins, the immune system, the vascular system, metabolic health, the environment and others all play a role in the disease process.”
While FDA-approved drugs that target amyloid are now available and in use, Ismail calls for a comprehensive approach to treating Alzheimer’s that involves multiple approaches.
“Understanding the complete underlying biology and related mechanisms is important to expand the scope of our treatment and prevention strategies,” said one expert on Alzheimer’s treatment. (iStock)
He recommends “a combination of therapies targeting different mechanisms, as well as lifestyle interventions, similar to how other major diseases such as diabetes, HIV/AIDS, and heart disease are treated.”
“Understanding the complete underlying biology and associated mechanisms is critical to expanding our range of treatment and prevention strategies,” Ismail said.
Potential Limitations
Espy also acknowledged the limitation that none of the published studies allowed access to individual-level data.
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“We can only work with published group-level data,” he told Fox News Digital. “Despite this limitation, the results were strongly supported.”
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Fox News Digital contacted Biogen and Eisai (the makers of Lecambi) and Eli Lilly (the makers of Kisunla) seeking comment.
