Researchers find protein that may help reverse Alzheimer's
Early studies on mice show promise in blocking the plaque that causes cognitive loss.
The discovery of two new protein fragments by researchers at Tel Aviv University may one day lead to a treatment to help reverse the effects of Alzheimer's disease.
The exact cause of Alzheimer's remains unknown, but previous research has shown that the condition is caused by plaque accumulations and tangles in neurons, which results in the death of brain cells. The proteins discovered by Professor Ilana Gozes and her colleagues could provide a protection against that plaque accumulation.
Gozes and her fellow researchers had previously discovered a potential drug called davunetide (aka NAP), which is a small peptide (a chain of amino acids) that in tests showed some ability to help people suffering from mild cognitive impairments (the stages prior to actual Alzheimer's). That drug failed in trials back in 2012, but as Gozes explained in a press release last month, the earlier work led them to continue exploring other proteins that might have similar functions. "This is the question that led us to our discovery," she said.
Like NAP, the new protein helps stabilize a part of the cell called the microtubule, which allows the transport of signals form one cell to another. Microtubules tend to collapse in Alzheimer's patients, so preserving them is critical to preserving brain function. Gozes found that the new protein helped maintain a portion of the microtubule called the tubulin. The researchers have called the protein TAU for tubulin-associated unit.
With that discovery in hand, Gozes and her colleagues tested two 10-month-old mice. One had dementia-like characteristics. They tested the TAU protein in the mouse and found that it protected the animal against further cognitive loss. It also regained some of its brain mass, an indication that brain degeneration was also reversed. As Gozes explained, "we clearly see here the protective effect of the treatment. We witnessed the restorative and protective effects of totally new protein fragments, derived from proteins critical to cell function, in tissue cultures and on animal models."
The research was published in a special supplemental issue of the Journal of Alzheimer's Disease.
This is just one of the many exciting new discoveries made recently in Alzheimer's research. A team from the University of Pennsylvania and Washington University in St. Louis has found that the drug citalopram, sold as the antidepressant Celexa, may reduce production of the plaque that causes Alzheimer's. Meanwhile, a team from Radboud University Medical Center in the Netherlands has found that people who have a bad night's sleep produce higher-than-normal levels of the amyloid-beta protein that is related to the plaque and tangles. "We think normal healthy sleep helps reduce the amount of (amyloid) beta in the brain and if your sleep is disturbed this decrease is prevented," the lead researcher told Reuters. Finally, scientists at New York University have found another compound that, in animal studies, cut the number of those amyloid proteins by more than 50%.
All of this research is in its early stages and won't be available for human tests for several years, but the scientists all expect that effective treatments for Alzheimer's may be available in the near future.
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