Cincinnati, Ohio. (Ivanhoe Newswire)— November is Alzheimer’s awareness month. For decades, scientists have focused on plaques in the brain, and treatments to remove those plaques. Now, a new finding has some researchers questioning the prevailing wisdom on why some people develop Alzheimer’s while others do not. It’s a theory that could lead to new treatments.
More than six million Americans are living with Alzheimer’s, and it’s predicted by 2050, those numbers will swell to 12.7 million, unless there is a breakthrough to prevent or cure it. For decades, scientists have believed that Alzheimer’s is caused by the protein A-beta-42, that causes a buildup of amyloids that are toxic to the brain. But now scientists at the Karolinska institute in Sweden, and University of Cincinnati say new research casts doubt on that theory.
Dr. Alberto Espay further explains that “In fact, by the age of 85, 60% of us have amyloids in our brains and only ten percent of us develop dementia. So that is a five-fold, lower prevalence of dementia that would have been predicted if amyloid was toxic.”
The researchers say instead of reducing or removing the plaques, treatment might involve increasing the levels of a soluble brain peptide called amyloid beta peptide. The researchers tested the theory by analyzing the brain scans of 600 people, all of whom had amyloid in the brain. Those who had normal cognition had higher levels of the amyloid beta protein than those who had dementia.
Dr. Espay says, “The replacement of these proteins that we’re losing may be the most important strategy in the future.”
Continuing to research new treatment options for older Americans impacted by Alzheimer’s.
The research team has formed an independent company to develop a replacement protein and is working to test it in animals. Dr. Espay says his team’s theory has been met with mixed reviews in the scientific community. Some say this explains why new therapies that work to remove plaques in the brain have had limited success. Earlier this year, the FDA approved the first drug in years that targets the removal of amyloid plaques after a period of heated debate.
Contributors to this news report include: Cyndy McGrath, Producer; Kirk Manson, Videographer; Roque Correa, Editor.
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Source:
https://www.medicalnewstoday.com/articles/327412
MEDICAL BREAKTHROUGHS
RESEARCH SUMMARY
TOPIC: ALZHEIMER’S RESTORING MISSING PROTEIN THE KEY?
REPORT: MB #4979
AMYLOID BETA BACKGROUND: Amyloid plaques are aggregates of proteins that have been misfolded and formed in the spaces between nerve cells. These cells are thought to affect Alzheimer’s disease because they are abnormally formed and develop in areas of the brain where memory and other cognitive functions are stored. They form when pieces of a protein called beta-amyloid form into a cluster. The beta-amyloid composed of 42 amino acids is chemically “stickier” than the other lengths and therefore is more likely to form plaques. Currently, it’s unclear how the beta-amyloid causes toxic damage to nerve cells, but there are many theories surrounding how it impact Alzheimer’s.
(Source: https://www.news-medical.net/health/What-are-Amyloid-Plaques.aspx)
AMYLOID BETA AND ALZHEIMER’S: The hypothesis that amyloid plaques have something to do with Alzheimer’s is because they develop in areas of our memory and cognitive functions and in Alzheimer’s disease, the brain cells that process and receive information degenerate and die. There are a few theories on why this happens to some people and not everyone. The “amyloid hypothesis” suggests that a microscopic brain protein fragment called beta-amyloid, a sticky compound that accumulates in the brain, is disrupting communication between brain cells and eventually killing them. Some researchers believe this while others believe Alzheimer’s could be caused by something else entirely. The amyloid plaques have gotten their status as a prime suspect to the cause of developing Alzheimer’s because they are stickier than other fragments that could be found in the same areas of plaque build up in the brain. Since they are sticky, they form small clusters called oligomers, then form chains of clusters called fibrils, then “mats” of fibrils called beta-sheets. The final stage is plaques, which contain clumps of beta-sheets and other substances.
(Source: https://www.alz.org/national/documents/topicsheet_betaamyloid.pdf)
NEW TECHNOLOGY: The cure for Alzheimer’s is still being researched, currently researchers are looking at several approaches for a cure, one being using the immune system. Several drugs are being tested as a way to prevent beta-amyloid from clumping into plaques or remove beta-amyloid plaques that have formed and help the body clear the beta-amyloid from the brain. The monoclonal antibodies are thought to be able to mimic the antibodies your body naturally makes as a part of your existing immune system. The antibodies are the response to foreign invaders and could potentially get rid of plaque build up in the brain. The FDA recently approved aducanumab for the treatment of some cases of Alzheimer’s disease.
FOR MORE INFORMATION ON THIS REPORT, PLEASE CONTACT:
ANGELA KOENIG
513-558-4625
or visit uc.edu for more on Espay’s research
If this story or any other Ivanhoe story has impacted your life or prompted you or someone you know to seek or change treatments, please let us know by contacting Marjorie Bekaert Thomas at mthomas@ivanhoe.com
