Scientists may have found a way to stop it Alzheimer’s disease damage By “dissolving” small protein clumps that are early triggers of disease, before the disease begins.
Alzheimer’s disease has long been associated with harmful tau protein fibrils that accumulate in the brain and interfere with cognitive function, but now researchers have discovered the soft, tiny clusters that appear first.
Dissolution of these nascent clusters may effectively prevent the formation of toxic fibrils. block the diseaseaccording to researchers at Tokyo Metropolitan University.
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Scientists led by Professor Rei Kurita used precise X-ray and fluorescence techniques in a laboratory setting to discover tiny “precursors” just a few tens of nanometers in size, according to a press release.
Because the small precursors were soft, the researchers were able to dissolve them. As a result, tau fibrils were not formed.
These results signal a change in the way scientists develop. Treatment for Alzheimer’s disease.
Rather than focusing on disrupting the final fibril formation, the new treatment could target earlier, reversible precursor stages, potentially preventing harmful structures from forming in the first place, according to the announcement.
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This strategy may eventually be applied in the following studies. Neurodegenerative diseases such as Parkinson’s disease.
This study has several limitations, primarily that it involved an in vitro biochemical model and did not involve humans or animals. It is unknown whether similar reversible clusters exist in human brain tissue.
Further research This is needed to find out whether disrupting these protein clusters is safe and can actually help treat the disease.
Dr. Mark Siegel, a senior medical analyst at Fox News, was not involved in the study but shared his reaction to the findings.
“There are three key structural components that are involved in the development of Alzheimer’s disease. beta amyloid proteintau protein and neuroinflammation,” he told Fox News Digital.
“There are already treatments on the market that target beta-amyloid buildup, and now there are targeted therapies that break down and destroy beta-amyloid. Accumulation of tau protein before the dreaded neurofibrillary tangles occur. ”
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Professor Siegel believes this “should have clinical value” and is better tolerated. other drugs Currently on the market.
“In the future, we’ll probably see triple therapy: anti-inflammatory, anti-beta amyloid, anti-tau,” he predicts.
Dr. Courtney Kloske, director of science at the Alzheimer’s Association of Chicago, also responded to the study in an interview with FOX News Digital.
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“This manuscript focuses on changing one of its characteristics, the structure of tau. brain protein “We’re looking for approaches that could play a role in Alzheimer’s disease and potentially slow or stop the progression of the disease,” said Kloske, who was also not involved in the study.
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“While this is promising basic research that could improve our understanding of the underlying mechanisms of disease, it is preliminary and additional research is needed to determine how these findings can be translated into human studies.”
Fox News Digital has reached out to researchers for comment.
