In recent months, a line of research focusing on specific amino acid chains from a class known as amyloid beta (Aβ) has shown great potential in treating Alzheimer’s Disease. Aβ deposits are known to cause the buildup of plaque in the brains of Alzheimer’s patients, affecting neurons and preventing brain cells from functioning properly. The exact role of Aβ is still not fully understood; however, scientists are gradually closing in on the answers – which could mean that effective treatments are not far behind.
Research published last year in Cell Reports found that a particular group of enzymes, known as HDACs, can interfere with the formation of synapses in the brain at the genetic level. By inhibiting the action of HDACs in test mice, it was possible to restore synaptic function. However, this study did not specifically target Aβ-related plaque buildup.
So far, studies aimed at preventing plaque buildup due to Aβ have produced mixed outcomes. Most of these have been unsuccessful in addressing this specific issue, although they have shown that Aβ plaque formation is only one piece in a complex puzzle. This line of research has suggested some preventive measures, however.
In August, scientists at the University of Florida found that a protein associated with the immune system, known as toll-like receptor 5 (TLR5), can be modified in such a way as to prevent the formation and buildup of amyloid plaques. Under normal circumstances, TLR5 detects bacterial pathogens, thereby activating antibodies.
When this receptor is damaged or not functioning properly, a person can be susceptible to a host of disorders, including lupus and respiratory inflammation. Researchers speculate that using TLR5 as a “decoy” could allow it to bind to Aβ, preventing it from forming the plaques that cause the degeneration associated with Alzheimer’s.
More recently, a research team from UCLA discovered a substance that might block Aβ plaques from attaching to brain cells in the first place. The molecule, found in a drug identified as “ALI6,” is non-toxic, able to cross the blood-brain barrier and block the receptors on brain cells that bind to Aβ plaques. They act as a “shield,” according to Dr. Lin Jiang, co-author of the study.
The best part: ALI6 is already approved for human use.
“Many drugs are aimed at preventing the b-amyloid proteins from accumulating and forming into plaques,” Jiang says. However, these treatments, while adequate for prevention, are less effective once the disease is apparent. Jiang adds, “When a person is diagnosed with Alzheimer’s, many of the b-amyloid plaques have already formed, so the time window for treatment is already closing.”
While these results are promising, further animal testing will be necessary before human trials begin. Currently, Alzheimer’s Disease is the sixth-leading cause of premature deaths in the U.S., affecting approximately 5.5 million individuals.