Researchers examined mammalian cells and found that blocking the interaction between alpha-synuclein and its chaperone proteins prompted alpha-synuclein accumulation similar to Lewy bodies, which are common in the brains of individuals with Parkinson's disease. The findings in the journal Nature suggest that chaperone protein dysfunction may be involved in Parkinson's development and could be a therapeutic target, researchers said.
Chaperone protein defects may prompt Parkinson's progression
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