Discovered a new therapeutic target for Parkinson’s disease.
Posted by giorgiobertin on July 24, 2023
Scientists at Northwestern University Feinberg School of Medicine have discovered a new mechanism by which mutations in a gene parkin contribute to familial forms of Parkinson’s disease. The discovery opens a new avenue for Parkinson’s therapies, scientists report in a new study. They found that mutations in parkin cause a breakdown of contacts between two key players in the cell: lysosomes and mitochondria.
Mitochondria are the main producers of energy in cells and lysosomes recycle the cellular debris that accumulates during the normal functioning of our cells. These organelles are particularly important in our brains because neurons are highly dependent on energy production by the mitochondria, and due to their activity, neurons produce an abundance of cellular debris that must be cleared by lysosomes.
Scientists have discovered that lysosomes provide important amino acids that support mitochondria function. However, they also found that in some forms of Parkinson’s disease, lysosomes cannot serve as a “helper” to the mitochondria because the contacts between the two organelles are disrupted. This results in dysfunctional mitochondria and ultimately the degeneration of vulnerable neurons in Parkinson’s disease.
“The results of this study suggest that dysregulation of mitochondria-lysosome contacts contributes to the pathophysiology of Parkinson’s disease“, ha affermato il prof. Krainc, del Department of Neurology, Northwestern University Feinberg School of Medicine. “We propose that the restoration of such mitochondria-lysosome contacts represents an important new therapeutic opportunity for Parkinson’s disease“.
Read the full text of the article:
Parkin regulates amino acid homeostasis at mitochondria-lysosome contact sites in Parkinson’s disease.
Wesley Peng, Leonie F. Schröder, Pingping Song, Yvette C. Wong, Dimitri Krainc.
Science Advances2023; 9 (29) DOI: 10.1126/sciadv.adh3347 19 Jul 2023
Fonte: Northwestern University Feinberg School of Medicine
Related articles:
Mitochondrial dysfunction in Parkinson’s disease: molecular mechanisms and pathophysiological consequences
Nicole Exner, Anne Kathrin Lutz, Christian Haass, Konstanze F Winklhofer
The EMBO Journal (2012)31:3038-3062
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This entry was posted on luglio 24, 2023 a 6:09 am and is filed under News-ricerca.
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