Scientists from the Albert Einstein College of Medicine have developed an experimental medication that reverses the major symptoms of Alzheimer’s disease. The researchers, who used mice for their research, found that the medication revitalized a cellular cleaning mechanism that eliminates unwanted proteins by recycling and digesting them. The research was reported in the “Cell” journal.
Ana Maria Cuervo, a professor and a study leader, explained that while discoveries in mice didn’t always play out the same way in human beings, the researchers were encouraged to learn that the cell-cleaning process that they had observed in mice also occurred in patients who suffered from Alzheimer’s.
A few decades ago, Cuervo, who also happens to be the Robert and Renée Belfer Chair for the Study of Neurodegenerative Diseases, found out about the existence of this cellular mechanism, scientifically referred to as CMA (chaperone-mediated autophagy). Since its discovery, Cuervo has published 200 papers on the mechanism’s role in disease and health.
From research, it is known that as individuals age, CMA grows less efficient. This heightens the risk that unwanted proteins will damage cells in the brain. Additionally, studies have shown that neurodegenerative ailments, including Alzheimer’s, are all characterized by the presence of toxic protein amassing in the brain of a patient.
The study observed a dynamic interplay between Alzheimer’s and the cellular mechanism, noting that the loss of CMA in neurons contributed to the ailment. These findings propose that medications that re-energize the mechanism may be useful in helping treat neurodegenerative ailments.
For their study, Cuervo and her team of researchers evaluated whether or not decreased CMA activity contributed to the progression of Alzheimer’s. This led to the discovery that the cellular mechanism was moderately hindered in individuals who were in the early stages of the disease, noting that this inhibition of cellular activity only grew in the brains of individuals in the advanced stages of Alzheimer’s.
In addition to this, the team of researchers also centered their focus on CMA activity in the neurons found in the brain, which led to the discovery that, in comparison to data from control animals, the CMA activity in neurons of the hippocampus was considerably reduced.
These findings were then used to create a new drug that could possibly be used to treat Alzheimer’s. Cuervo pointed out that the drug rejuvenated the efficiency of CMA by improving levels of LAMP2A receptors. An increase in these receptors, which are produced from lysosome membranes, was found to boost CMA activity.
This research was backed by the Backus Foundation, Michael J. Fox Foundation, and the Rainwater Charitable Foundation as well as the National Institutes of Health, among other organizations.
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