Hope for nipping Alzheimer’s in the bud
Wouldn’t it be wonderful to be able to nip Alzheimer’s disease in the bud before it got started — or at least nab it in its early stages?
This has, of course, been the dream of researchers and medical professionals for several decades. Now it appears the dream might soon become a reality.
Last month, an article published in the Proceedings of the National Academy of Sciences reported on the findings of a research study, conducted at the University of Washington in Seattle, which tested the effectiveness of a new synthetic protein in stopping the progression of Alzheimer’s in its early stages.
The study targeted beta-amyloid, which is thought to be responsible for memory loss and general cognitive decline.
For several decades, it was thought that the beta-amyloid plaques — the large clumps of beta-amyloid that accumulate around neurons — were the cause of the classic symptoms associated with Alzheimer’s.
However, over the past few years, evidence has been mounting that the plaques themselves are not the culprit. The toxicity of beta-amyloid lies in an earlier stage of the process of plaque formation.
Beta-amyloid in its simplest form is called a “monomer.” Monomers clump together to form what are called “oligomers.” The oligomers go on to form larger units known as “fibrils,” which then cluster together and form plaques.
The only stage in which beta-amyloid is harmful appears to be in the oligomer stage. Not only do oligomers cause damage to neurons (brain cells), but one form of oligomer is capable of spreading by converting surrounding non-toxic monomers into toxic oligomers. This ability to act as a “seed” from which new toxic oligomers spring is perhaps the most dangerous aspect of beta-amyloid oligomers.
Another aspect of beta-amyloid oligomer activity is its association with inflammation. Inflammation in the brain is one of the earliest signs that Alzheimer’s is setting in, even before the appearance of the beta-amyloid plaques.
Research conducted between 2012 and 2015 has uncovered many ways in which beta-amyloid oligomers give rise to inflammation, though the relationship between the two is not absolutely clear.
It is important to note that none of the other forms of beta-amyloid monomers, fibrils or plaques is associated in any way with inflammation, and they are therefore not contributors to the development of Alzheimer’s.
Aiming for a new target
The new approach to stopping Alzheimer’s targets beta-amyloid in its toxic oligomer stage.
Researchers created a new synthetic protein (known as a peptide). The synthetic protein mimics the shape of the oligomers and wraps itself around them, thus shielding the surrounding area from their toxic effects, and also preventing them from “infecting” non-toxic forms of beta-amyloid.
The study tested the new protein on animal models, which documented a 40% reduction in oligomer levels within 24 hours. The synthetic protein was also tested on the common roundworm or nematode (C. elegans) with positive results.
What does this mean for humans? First, researchers suggest that the new protein can be used to develop a test that measures the level of toxic beta-amyloid oligomers in the brain and thus provide an early diagnosis of Alzheimer’s before the symptoms appear.
Second, research is already under way to develop a treatment that will trap and remove the toxic beta-amyloid oligomers before they have a chance to do further damage. This sounds very promising and gives us every reason to be hopeful.
Veena J. Alfred, Ph.D., is a Certified Dementia Practitioner and CEO/Administrator of AlfredHouse Assisted Living.