In terms of Alzheimer’s research, the ultimate goal is to find a cure. Although no new drugs have been developed for Alzheimer’s in 15 years, the research has continued to evolve at a rapid pace.
Recently, scientists at Washington University made the headlines after they successfully removed one of the hallmarks of Alzheimer’s from mice. Reported as a potential ‘game changer’ for drug trials, this new antibody treatment could significantly reduce levels of amyloid plaques in the brain.
Study Finds New Potential Alzheimer’s Treatment
As early as 20 years before Alzheimer’s symptoms develop, amyloid beta plaques may begin to accumulate in the brain. A key hallmark of Alzheimer’s, these plaques are believed to cause both cell death and tissue loss in the brain. Clusters of the protein known as beta-amyloid, these sticky plaques interfere with nerve cells.
As mentioned, researchers at Washington University School of Medicine recently developed an antibody that may target plaques. A number of recent clinical trials have tested antibodies in regards to plaques, but none have been successful. In fact, none have made it past the trial phase. These trials also yielded various side effects.
Unlike these past attempts, this new approach may address potential side effects, while interfering with plaques before symptoms develop. In this study, instead of focusing on antibodies that match amyloid beta proteins, the researchers studied a smaller component within them, known as APOE. This class of proteins supports the metabolism and transportation of fats in the bloodstream.
Testing a number of antibodies in mice, all which were good fits for human APOE, they made an exciting discovery. The antibodies successfully attracted other immune cells which then attacked the APOE protein. One antibody in particular, HAE-4, was particularly effective.
After just six weeks, the mice treated with this antibody experienced an approximate 50 percent reduction in the level of amyloid beta proteins. Best of all, the APOE found in plaques differed from the form of APOE commonly found in the bloodstream. This means that the antibody does not appear to interfere with the critical fat-eliminating role of APOE.
The goal is to continue testing this discovery in the hopes of stopping early changes in the brain before significant damage occurs. These findings were published in the Journal of Clinical Investigation.
Plaque Build-Up, Alzheimer’s, and the Immune System
This is not the first time the immune system has been shown to play a potential role in reversing the toxic build-up of plaques in the brain. In a 2015 study, published in Neuron, researchers made a promising discovery. By ‘rebalancing’ the immune response, the researchers were able to clear the brain of beta-amyloid plaques. In turn, this helped to restore brain cell damage and memory loss.
More recently, researchers at the University of Colorado Anschutz Medical Campus focused on the pathology of Alzheimer’s in relation to immune function. More specifically, they were interested in how the brain and the rest of the body communicate.
After testing 173 middle-aged and older adults, they made an unexpected discovery. They found a clear association between inflammation biomarkers and markers of Alzheimer’s associated pathology. These biomarkers were found in the cerebrospinal fluid and blood plasma.
These findings were published in the Journal of Alzheimer’s Disease.
Reducing Plaques in the Brain
Although you may feel powerless to Alzheimer’s, the research has continued to show otherwise. Large, reliable studies have consistently reported that active individuals who eat healthy are significantly less likely to develop symptoms of dementia.
In one 2016 study, researchers at the University of California Los Angeles found that a healthy lifestyle reduces the build-up of both tau and amyloid proteins in the brain. It was stated that a healthy body mass index, an active lifestyle, and a Mediterranean diet all lowered levels of plaques.
Lowering levels by between one and three percent, this may be enough to delay dementia onset.
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