Rethinking what causes Parkinson’s: Studies suggest we may be looking in the wrong place

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Image: Tatiana Shepeleva/Shutterstock

During her time as a postdoc at the University of Basel in Switzerland, Sarah Shahmoradian decided to study the abnormal aggregates of protein that develop inside nerve cells and contribute to Parkinson’s disease.

“We were originally looking for fibrils,” Shahmoradian says, “but unexpectedly, we found an abundance of . . . mitochondria, other organelles, and lipid membranes [in the Lewy bodies].” The researchers also found evidence of lysosomes, organelles that facilitate cellular waste removal.

The study is one of many that raise questions about the prevailing idea that α-synuclein accumulation is the underlying cause of the neurodegeneration in Parkinson’s disease. Rather, α-synuclein buildup may be just one symptom of a more fundamental problem: the cells’ inability to break down excess lipids and proteins, including α-synuclein. Some Parkinson’s patients carry mutations in genes associated with lysosomal function, and studies in mice have revealed that natural aging leads to the build-up of lipids associated with Parkinson’s disease. These findings have led a small but growing set of scientists to propose that for a vast majority of Parkinson’s patients, the disease is fundamentally a cellular machinery problem, not a protein problem.

Related article:  Was it 'bad luck'—not ancient humans—that drove Neanderthals to extinction?

Read full, original post: Is It Time to Rethink Parkinson’s Pathology?

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