It is estimated that about 44 million people worldwide are currently living with Alzheimer's disease. One of the most influential research articles on Alzheimer’s states that the disease is caused by the buildup of amyloid plaques in the brain. However, new research has discovered that the disorder is caused by a decline in levels of a soluble protein called amyloid beta. The investigation by Science Magazine is published in the Journal of Alzheimer's Disease.
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The original research was published in 2006 and has been cited in over 2,000 articles since then. The study suggested that the formation of amyloid plaques in the human brain is the main cause of senile dementia. Amyloid plaques are clumps of a sticky protein called amyloid-beta that form in the spaces between nerve cells. Experts have believed that these abnormally configured proteins play a key role in Alzheimer's disease. They are thought to first develop in the areas of the brain related to memory and other cognitive functions.
In the current study, scientists from the University of Cincinnati and Karolinska Institute analyzed the concentration of amyloid plaques and amyloid-beta proteins in two groups. The first group consisted of people that had a very high risk of Alzheimer’s according to the 2006 study. The researchers found mutations signaling the development of amyloid plaques in the future. The second group was comprised of healthy individuals.
The researchers observed that, in both cases, individuals with low concentrations of soluble amyloid-beta protein were at a bigger risk of dementia. In contrast, those more likely to have amyloid plaques in their brain in the future but also high concentrations of amyloid-beta protein demonstrated normal brain activity.
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“What we found was that individuals already accumulating plaques in their brains who are able to generate high levels of soluble amyloid-beta have a lower risk of evolving into dementia over a three-year span,” says study author Alberto Espay, Professor of Clinical Division Director at UC College of Medicine.
The researchers point out that the concentration of soluble amyloid-beta protein decreases when it becomes insoluble amyloid plaques because of many stress factors that alter its metabolism. They further note that many past clinical trials concentrated on treating Alzheimer’s aimed to remove amyloid plaques. However, barring one, none of those strategies proved to be effective against the disease.
The one trial that was successful in providing relief against Alzheimer’s uses a drug called lecanemab, which increases the concentration of soluble amyloid-beta protein apart from removing amyloid plaques. The researchers say that the trials in which the level of amyloid-beta protein went down produced negative results.
“I think this is probably the best proof that reducing the level of the soluble form of the protein can be toxic,” said Sturchio, first author of the report and adjunct research instructor at UC’s College of Medicine. “When done, patients have gotten worse.”
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Previous research had found that people with high levels of soluble amyloid-beta were cognitively normal irrespective of the buildup of plaques in the brain. They also found that individuals with low levels of protein were more likely to have cognitive impairment.
Now, the research team believes that if their hypothesis about Alzheimer’s turns out to be true, then the same theory can be applied to other degenerative brain disorders like Parkinson’s disease, Creutzfeldt-Jakob disease, etc. For example, many studies claim that Parkinson’s is caused by the buildup of insoluble deposits called Lewy bodies in the brain. According to the researchers, Parkinson’s may actually be caused by low levels of soluble alpha-synuclein protein instead of Lewy bodies, as they are also formed when the protein hardens and becomes insoluble.
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Currently, the team is focused on determining whether increasing the levels of soluble amyloid-beta in the brain is a beneficial therapy for patients with Alzheimer’s. According to professor Espay, we might be able to treat degenerative disorders like Alzheimer’s more effectively if we try and increase the level of the soluble protein in the brain via medicines rather than focusing on removing the insoluble deposits.
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