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Are we wrong about Alzheimer’s? Researchers question the theory that influenced the new discovery.

Alzheimer's dementia concept

Scientists at the University of Cincinnati say it restores brain proteins. It̵

7;s not a plaque amyloid removal. It should be the goal of Alzheimer’s treatment.

Experts estimate that more than 6 million Americans are living with Alzheimer’s dementia. But a recent study led by the University of Cincinnati sheds new light on the disease and a highly controversial new drug therapy.

A UC-led study, conducted in collaboration with the Karolinska Institute in Sweden, argues that the treatment for Alzheimer’s may involve normalizing levels of a specific brain protein called amyloid-beta peptide. Soluble original to keep the brain healthy But sometimes it hardens into “brain stones,” or clumps called amyloid plaques.

Research published in the journal medical clinic (published by lancet) comes from the FDA’s conditional approval of a new drug, aducanumab, that treats amyloid plaques.

Alzheimer's theory, new discoveries

Study results graph. Credits: Life Science Animation.

“It’s not plaque that causes cognitive impairment,” said Alberto Espay, a member of the UC Gardner Neuroscience Institute, “Amyloid plaques are a consequence of Alzheimer’s disease,” said Alberto Espay, senior author and professor of neurology at UC.

Alzheimer’s disease has become widely known as However, more than 100 years ago, the disease slowed brain function and memory loss. Scientist Alois Alzheimer has identified plaque in the brains of patients with the disease for the first time.

Since then, Espay says scientists have focused on treatments to remove plaque. But, he said, the UC team saw it differently: The cognitive impairment could be caused by a reduction in the soluble amyloid-beta peptide instead of the corresponding amyloid plaque buildup. to test their hypothesis They analyzed brain and cerebrospinal fluid scans from 600 people enrolled in the Alzheimer’s Disease Neuroimaging Initiative study. All of them had amyloid plaque. From there, they compared the amount of plaque and the level of peptides in normal cognitive individuals with those with cognitive impairment. They found that regardless of the amount of plaque in the brain, Individuals with high levels of peptides are cognitively normal.

Alberto Espey

Alberto Espay, MD, MSc, professor of neurology at the UC College of Medicine and director and president of the James J. and Joan A. Gardner Family Center for Parkinson’s and Movement Disorders. credit: Colleen Kelley/ UC Brand + Creative

They also found that higher levels of soluble amyloid-beta peptides were associated with larger hippocampus. which is the area of ​​the brain that is most important for memory

According to the authors, as we age, most people develop amyloid plague, but few develop dementia. In fact, by age 85, 60% of people will develop the disease, but only 10% will develop dementia.

Co-author Kariem Ezzat, from the Karolinska Institute, said: “The key finding from our analysis is that the symptoms of Alzheimer’s disease depend on the depletion of normal proteins. which is in a soluble state instead of being assembled into a sheet of metal

The most relevant future treatment for Alzheimer’s disease program is the replenishment of these brain soluble proteins to normal levels, Espay said.

The research team is working to test their findings in animal models. if successful Future treatments could differ greatly from treatments from the past two decades. Treatment, Espay says, may consist of adding soluble proteins in a way that keeps the brain healthy while preventing the protein from clotting into plaques.

Cited from: June 28, 2021, medical clinic.
doi: 10.1016/j.eclinm.2021.100988

Co-authors are Andrea Sturchio, University of Cincinnati, and Samir EL Andaloussi, Karolinska Institute.

The research was funded by the UC Gardner Neuroscience Institute.

The authors revealed that they recently co-founded REGAIN Therapeutics, which owns a patent application covering synthetic, synthetic, water-soluble, insoluble peptide analogs as replacement treatments in protein-bound diseases.

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