Researchers hope to learn why the protein alpha-synuclein accumulates in glial cells in MSA and neuronal (nerve) cells in Parkinson’s disease. Recent studies have demonstrated that the alpha-synuclein taken from brain tissue of patients with MSA is a potent inducer of alpha-synuclein clumping when injected into the brain of experimental animals. One exciting area of ongoing research is aimed at blocking the spread of this protein clumping problem throughout the brain.
Recent research suggests that abnormal alpha-synuclein accumulation in nerve cells and their supporting cells leads to cellular dysfunction and progressive loss of nerve cell function (neurodegeneration). Using cell models of MSA, scientists were able to show that damage to mitochondria (cellular “power plants”) and the generation of abnormal alpha-synuclein aggregates may contribute to the development of MSA. Research in animal models may determine if drugs that reduce the abnormal alpha-synuclein accumulation might be promising treatments for MSA.
Https://www.ninds.nih.gov/Disorders/Patient-Caregiver-Education/Fact-Sheets/Multiple-System-Atrophy#3145_5
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