After decades of disappointing findings in new Alzheimer’s disease research, scientists have hit on what many experts believe is a promising new way to reverse the condition that could be a game changer in treating the memory-robbing disorder.
A new Cleveland Clinic study found that amyloid protein plaques that accumulate in the brain, which are hallmarks of Alzheimer’s, were eliminated when a researchers removed a naturally occurring enzyme — called BACE1 — from the brains of mice genetically engineered to have a rodent form of the disease.
“To our knowledge, this is the first observation of such a dramatic reversal of amyloid deposition in any such study of Alzheimer’s disease mouse models,” senior researcher Riqiang Yan said in a press release about the study, which was published in the Journal of Experimental Medicine.
According to the Alzheimer’s Association, plaque buildup is a key contributor to cell death and tissue loss in those with Alzheimer’s disease. If the findings hold up in follow-up clinical studies, they could pave the way for new therapies that could reverse the brain disorder.
Yan told Newsmax Health that he and his team at the Cleveland Clinic found that when the BACE1 enzyme was removed, existing plaque in the brains of the mice disintegrated. But he added that the researchers also found that the formation of amyloid plaque also stalled, suggesting BACE1 might be the basis for a new treatment and also preventive strategies.
Yan added that removal of the enzyme also improved learning and memory in the mice.
“I’m one of the original discoverers of BACE1, and this discovery was published in 1999 in Nature,” he told Newsmax Health. “Since then, I’ve been trying to use mouse [studies] to understand how to inhibit BACE1 for the best benefit of Alzheimer patients. We aim to provide guidance [for a] human study.”
BACE1, known as beta-secretase, clings to what’s called the amyloid precursor protein which cases the production and buildup of plaques that gum up the action of brain cells. This buildup has been linked to Alzheimer’s, which spurred Yan’s research to try and isolate BACE1.
“Reducing BACE1 levels in the offspring mice also reversed other Alzheimer’s hallmarks, such as microglial cell activation and formation of abnormal neuronal processes. Moreover, reduced BACE1 was associated with improved learning and memory in mice,” Yan said.
Yan and his colleagues at Cleveland Clinic gradually removed BACE1 from mice as they aged. The mice showed healthy development over time and by the time they were 10 months old — the equivalent of 50 years in humans — they no longer had any amyloid plaque remaining.
Most experts believe that Alzheimer’s develops as a result of complex interactions among genes and other risk factors, including the buildup of protein plaques in the brain.
Dr. Keith Fargo, Alzheimer’s Association director of scientific programs and outreach, notes, that the good news is that some of those risk factors can be counteracted by healthy habits — such as eating a healthy diet, exercising regularly.
“Age, family history, and heredity are all risk factors we can’t change. Some of the strongest evidence links brain health to heart health. This connection makes sense, because the brain is nourished by one of the body’s richest networks of blood vessels, and the heart is responsible for pumping blood through the blood vessels to the brain,” Fargo tells Newsmax Health.
“The risk of developing Alzheimer’s disease or vascular dementia appears to be increased by many conditions that damage the heart and blood vessels. These include heart disease, diabetes, stroke, high blood pressure, and high cholesterol. Studies of donated brain tissue provide additional evidence for the heart-head connection. These studies suggest that plaques and tangles are more likely to cause Alzheimer’s symptoms if strokes or damage to the brain’s blood vessels are also present.”
Yan tells Newsmax Health his hope is that his research points the way to effective new therapies that will be available for Alzheimer’s and dementia patients in the next decade.
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