Parkinson’s disease is characterized by the death of the neurons responsible for the control and coordination of movements, but in 90% of cases the reason for this is unknown, while in around 10% of patients it could be explained by a genetic predisposition. New research has revealed that the protein galectin-3 (gal3) may play a key role in the onset and progression of Parkinson’s.
This protein had already been linked to other neurodegenerative diseases such as Alzheimer’s and metabolic disorders, so it could become a therapeutic target when developing new and better treatments. The study was carried out by a team of researchers from the Seville Institute of Biomedicine (IBiS), in collaboration with the University of Lund (Sweden) and Imperial College London, who have published their findings in Acta Neuropathologica.
These scientists carried out a study of the brains of patients who had died with Parkinson’s and of transgenic mice that lacked the gal3 protein, which allowed them to demonstrate that there was a direct association between the presence of gal3 and the formation of Lewy bodies that are Toxic accumulations of proteins that appear in the neurons involved in movement that are affected by Parkinson’s, and also in other types of nerve cells in the brain that are involved in memory and thought.
If the effects observed in animals were replicated, a treatment against galectin-3 could be effective for more years and the patient with Parkinson’s could maintain a better quality of life.
The researchers found that when transgenic mice without gal3 were subjected to a model of Parkinson’s disease, they neither developed motor symptoms nor experienced the loss of neurons. “It is important to note that these mice did not develop any type of symptoms and their neurons remained apparently healthy, despite accumulating Lewy bodies. This indicates that by eliminating gal3, we were able to delay and slow down the progression of the disease”, highlighted Dr. Juan García Revilla, Researcher of the Neuronal Aging group of the Seville Institute of Biomedicine (IBiS) and one of the authors of the study.
A treatment against galectin-3 could fight Parkinson’s
This discovery opens new possibilities to develop therapies targeting the gal3 protein that are effective in alleviating the symptoms of Parkinson’s. “If we could translate these results to the human level, it would be an important advance in the treatment of Parkinson’s, since there are currently no therapies that can change or delay the evolution of the disease. We are confident that the relevance of gal3 in humans is also high, since this protein is widely present in the brains of patients with Parkinson’s”, adds Dr. García Revilla.
Complete neuronal protection against Parkinson’s has been observed in mice, although the specialist warns that there is still a long way to go to develop a therapy that can be administered to patients. “We believe that a treatment against galectin-3 could be tremendously useful for the treatment of the disease. If the effects were replicated in animals, symptomatic treatments could be effective for more years and the patient could maintain a better quality of life.”
Dr. García Revilla affirms that his “discovery helps to know more about the progression of the pathology and the relationship between Lewy bodies and the death of neurons”, and that they have also proven “that it is possible to separate both things and that we can protect neurons during disease.” As he explained, there are already drugs directed against galectin-3 in other diseases: “Our previous study in Alzheimer’s disease has been the basis for a clinical trial against gal3 which, for the moment, is very promising, although it is in phases. very initial ”, he adds.
“We are confident that a similar trial could have a big impact in Parkinson’s disease. This study is a big step forward in our understanding of the disease, but of course there is still a lot of work to be done”, he concludes. The study has been led by Drs. José Luis Venero (IBiS), Tomas Deierborg (Lund University) and Francesco A. Aprile (Imperial College London).
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