A new study from the University of Cincinnati shows that increases in protein levels with new Alzheimer’s drugs can explain the slowing of cognitive impairment at least as well as the reduction in amyloid plaques.
Published in the journal Brain, the study challenges the assumption that new Alzheimer’s drugs help with cognitive improvement by removing amyloid plaques. Instead, the study posits that the drugs also increase levels of a protein called amyloid-beta 42 (Aβ42), which may be at least partly, if not entirely, behind the cognitive improvement.
“Most of us will accrue amyloid plaques in our brains as we age, and yet very few of us with plaques go on to develop dementia,” said Dr. Alberto Espay, professor of neurology in the UC College of Medicine, who led the study. “Yet the plaques remain the center of our attention in biomarker development and therapeutic strategies.”
“If the problem with Alzheimer’s is the loss of the normal protein, then increasing it should be beneficial, and this study showed that it is,” Espay explained. “The story makes sense: Increasing Aβ42 levels to within the normal range is desirable.”
Fox News reports on the new study that challenges longstanding assumptions about what causes Alzheimer’s. Here’s the start of the story:
Boosting a specific protein in the brain could help slow the progression of Alzheimer’s disease, a new study has found.
The longstanding theory is that Alzheimer’s occurs when a protein called amyloid-beta 42 (Aβ42) transforms into plaques that build up in the brain, causing damage to neural cells and leading to cognitive decline.
Researchers from the University of Cincinnati have challenged that assumption, instead suggesting that the disease is caused by low levels of healthy, functioning Aβ42, according to a UC press release.
They based this hypothesis on the fact that newly approved monoclonal antibody medications — including lecanemab (Leqembi) and donanemab (Kisunla) — have had the unintended outcome of raising levels of the protein in the brain.
“The new Alzheimer’s treatments, which were designed to remove amyloid plaques, unintentionally raised Aβ42 levels, and this may explain their positive effects on cognition as much as — or better than — amyloid reduction,” lead study author Alberto J. Espay, MD, professor of neurology at the Gardner Family Center for Parkinson’s disease and Movement Disorders at UC, told Fox News Digital via email.