Absence of SMG1 protein could lead to Parkinson`s
Washington: A new study has suggested that the absence of a protein called SMG1 - identified as a Regulator of Parkinson's disease-associated alpha-Synuclein Ttrough siRNA Screening - could aid in the development of Parkinson's and other related neurological disorders.
The study led by the Translational Genomics Research Institute (TGen) screened 711 human kinases (key regulators of cellular functions) and 206 phosphatases (key regulators of metabolic processes) to determine which might have the greatest relationship to the aggregation of a protein known as alpha-synuclein, which was earlier implicated in Parkinson's disease.
Senior author Dr. Travis Dunckley, a TGen Assistant Professor, said that identifying the kinases and phosphates that regulate this critical phosphorylation event may ultimately prove beneficial in the development of new drugs that could prevent synuclein dysfunction and toxicity in Parkinson's disease and other synucleinopathies.
Synucleinopathies are neurodegenerative disorders characterized by aggregates of a-synuclein protein. They include Parkinson's, various forms of dementia and multiple systems atrophy (MSA).
Dr. Dunckley and collaborators used the latest in genomic technologies, to find that expression of the protein SMG1 was "significantly reduced" in tissue samples of patients with Parkinson's and dementia.
He said that these results suggest that reduced SMG1 expression may be a contributor to a-synuclein pathology in these diseases.
The study has been published in the journal PLOS ONE.
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