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A recent study conducted by the Indian Institute of Technology (IIT) Mandi has unveiled a groundbreaking discovery regarding the role of a protein, Alpha-synuclein, in both the progression of Parkinson’s disease and regular brain function. Published on Thursday, the findings shed new light on potential therapeutic approaches for Parkinson’s and underscore the intricate interplay between molecular mechanisms and brain health.
Parkinson’s disease, a neurodegenerative disorder, has been witnessing a global surge, with experts projecting a significant increase in cases in India by 200-300 per cent over the next two to three decades.
Led by an international team of experts, the study employed a diverse array of techniques to investigate the nature of Alpha-synuclein and its implications in Parkinson’s disease. Alpha-synuclein, abundantly present in the brain, undergoes phosphorylation, a process involving the attachment of phosphate groups to specific amino acids, particularly serine-129, in patients with Parkinson’s and related conditions.
Phosphorylation, likened to a molecular master switch, intricately regulates the activity of proteins, influencing molecular interactions crucial for the progression of Parkinson’s disease. Notably, inhibiting phosphorylation at the 129th position of Alpha-synuclein holds the potential to halt the disease progression.
“This important study changes how we think about a protein change linked to Parkinson’s disease. It shows that this change, called phosphorylation at a certain site on the alpha-synuclein protein, is not just a disease marker but also crucial for normal brain work,” remarked Dube Dheeraj Prakashchand, emphasizing the significance of the findings.
The research, conducted through biochemical assays, protein analysis, and gene studies on mouse models, revealed that preventing the phosphorylation of Alpha-synuclein significantly impairs normal brain function. This suggests that phosphorylation at serine-129 may serve as a switch triggered by brain cell activity to initiate vital signaling pathways.
The study’s findings hold promising implications for the development of drugs or gene therapies aimed at maintaining optimal levels of phosphorylated Alpha-synuclein in specific brain regions. Moreover, molecules can be engineered to modulate the connections involving phosphorylated serine-129 to treat Parkinson’s disease effectively.
Moving forward, phosphorylated serine-129 models may serve as valuable tools for evaluating the impact of Parkinson’s medications on Alpha-synuclein phosphorylation, paving the way for more targeted and effective therapeutic interventions.
The study not only advances our understanding of Parkinson’s disease but also opens new avenues for therapeutic strategies that prioritize both disease management and brain health maintenance.
