A group of researchers from the Institute of Biomedicine in Seville (IBiS), in collaboration with the University of Lund (Sweden) and Imperial College London, identified an important relationship between a protein called galectin-3 (gal3) and the Parkinson’s disease.
According to the results, recently published in the journal Acta Neuropathologica This plays a crucial role in the development and progression of this neurodegenerative disease, making it a potential therapeutic target of great interest for the treatment of the disease.
The research highlights the role gal3 protein in Parkinson’s disease, known for the death of neurons responsible for coordinating movement. This protein is known to be involved in other neurodegenerative processes (such as Alzheimer’s) and metabolic diseases, which increases its relevance in the field of medical research.
By studying the brains of deceased patients with Parkinson’s disease and transgenic mice lacking the gal3 protein, the direct association between the presence of gal3 and the formation of Lewy bodieswhich are toxic accumulations of proteins that appear in neurons affected by Parkinson’s.
These findings are significant, as when transgenic mice lacking gal3 were subjected to a model of Parkinson’s disease, they did not develop motor symptoms or experience neuron loss.
“It is important to note that these mice did not develop any kind of symptoms and their neurons remained apparently healthy despite accumulating Lewy bodies. This indicates that, by eliminating gal3, we managed to delay and slow down the progression of the disease”, emphasizes the Juan Garcia Revillaauthor of the study and researcher in the Neuronal Aging group at the Institute of Biomedicine in Seville (IBis).
“If we could transfer these results to the human level, it would be an important advance in treatment of Parkinson’s, since currently there are no therapies that can alter or delay the evolution of the disease. We are confident that the relevance of gal3 in humans is also high, as this protein is widely present in the brains of Parkinson’s patients.”
This discovery opens new perspectives for the therapy development targeting the gal3 protein, which opens the door to new possibilities in the management, mitigation and treatment of Parkinson’s disease.
The path to possible treatment
“The animal model was a pleasant surprise for the complete neural protection that we observe”, reaffirms the researcher. However, the development of a possible treatment is still long.
“We believe that a treatment against galectin-3 could be extremely 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 better health. quality of life”.
However, explains the specialist, there is still much to learn about Parkinson’s disease: “We do not know the causes that initiate Parkinson’s disease, but our discovery helps to learn more about the pathology progression and the relationship between Lewy bodies and neuron death. In turn, we proved that it is possible to decouple the two and that we can protect neurons during disease.”
The animal model was a pleasant surprise due to the complete neuronal protection we observed.
According to the researcher, there are already drugs directed against galectin-3 in other diseases. “Our previous study on Alzheimer’s disease formed the basis for a clinical trial against gal3 that is currently showing great promise, although it is in the early stages,” he adds.
“We are confident that a similar study could have a big impact on Parkinson’s disease. This study is a huge step forward in our understanding of the disease, but it is clear that there is still much work to be done.”
The study was conducted by Drs. José Luis Venero (IBiS), Tomas Deierborg (Lund University) and Francesco A. Aprile (Imperial College London) and was funded nationally by the Spanish Ministry of Science and Innovation and Michael J. Fox The Michael J. Fox Foundation for Parkinson’s Research.
Reference:
Juan Garcia-Revilla, et al. “Galectin-3 shapes toxic alpha-synuclein strains in Parkinson’s disease”. Acta Neuropathologica (2023)