Deficits in Cellular Recycling May Be Key in Better Understanding Parkinson Disease

“It’s a time of tremendous revolution in Parkinson’s disease,” says Un J. Kang, MD, H. Houston Merritt Professor of Neurology and Chief of the Division of Movement Disorders at Columbia University Medical Center. Significant progress has been made in understanding the multifactorial pathogenesis of this neurodegenerative disease, with a focus on genetic and environmental factors, but the exact pathogenesis is still unknown. Current therapies treat certain symptoms but do not stop disease progression.

One exciting avenue of research that may lead to targeted treatment is “autophagy,” or “self-eating,” based on the term’s Greek roots. Autophagy is important for the removal of abnormal proteins and damaged organelles, and dysregulation of autophagic pathways has been observed in the brains of people with Parkinson’s disease. Abnormal autophagy produces, as Dr. Kang describes, “deficits in cellular recycling” that essentially clog the cellular machinery. The discovery of therapeutic agents that regulate authophagic activity could potentially protect against neurodegeneration in Parkinson’s and other neurodegenerative diseases.

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