How Shocking Study Finds Decreased Proteins – Not Amyloid Plaques – Cause Alzheimer’s Disease

 


New research from the University of Cincinnati (UC) supports the hypothesis that Alzheimer's disease is caused by a decline in levels of a specific protein, in contrast to a prevalent theory that has recently been called into question


Questioning The Dominant Hypothesis



The protein known as amyloid beta was the subject of this study. In normal circumstances, the protein in the brain performs its functions in a soluble form, which means that it dissolves in water. However, it occasionally hardens into clumps or amyloid plaques. For more than a century, the conventional wisdom in the field of Alzheimer's research stated that the accumulation of amyloid plaques in the brain was the cause of the disease. However, his colleagues hypothesized that the decline in brain levels of soluble amyloid-beta was the only cause of plaques. These levels decrease when the normal protein forms abnormal amyloid plaques in response to biological, metabolic, or infectious stress. 


The paradox is that so few of us who have plaques in our brains go on to develop dementia, despite the fact that so many of us get older. He is a doctor at UC Health, a professor of neurology at the UC College of Medicine, and the director and endowed chair of the UC Gardner Neuroscience Institute's James J and Joan A Gardner Family Center for Parkinson's Disease and Movement Disorders. However, when it comes to the creation of biomarkers and therapeutic approaches, the plaques continue to be the focus of our attention


According to researchers at the University of California, San Diego, patients have gotten worse during clinical trials aimed at reducing amyloid plaques in the brain. A positive preliminary study by Biogen and EISA I really eased back the movement of Alzheimer's disease


Research Results

Results of Previous Studies Conducted by the team, it was revealed that individuals with high levels of soluble amyloid-beta were cognitively normal regardless of the presence of plaques in the brain, whereas individuals with low levels of the protein were more likely to suffer from cognitive impairment. 

 

The current study examined the levels of amyloid beta in a subset of patients with mutations that are thought to increase their risk of Alzheimer's disease by predicting an over expression of amyloid plaques in the brain. 

 

Sturchio stated, "These mutations were one of the strongest supports for the hypothesis of amyloid toxicity". We looked into that group of people because it has the most important data. 

 

The researchers observed results that were comparable to those found in the study of the general population—even among the patients thought to have the highest risk of developing Alzheimer's disease.

 

According to E S P A Y, "what we found was that people who are already accumulating plaques in their brains and who are able to generate high levels of soluble amyloid-beta have a lower risk of evolving into dementia over a three-year span". 

 

As long as the baseline level of soluble amyloid beta in the brain remains above 270 picograms per milliliter, the study found, individuals can maintain a cognitively normal status regardless of the amount of amyloid plaques in their brains. 

 

"A neurodegenerative process is caused by something we lose, amyloid beta, rather than something we gain, amyloid plaques, if you are detached from the biases that we've created for too long", E S P A Y stated. Degeneration is a loss process, and what we lose becomes far more significant 

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