Increasing protective protein suppresses Parkinson's-linked buildup, more than doubling lifespan in mouse model
Yale researchers have successfully used a protective protein to prevent the buildup of toxic alpha-synuclein in a mouse model of Parkinson's disease. This intervention more than doubled the lifespan of the mice, offering a potential pathway for future human therapies.
Why it matters
This discovery provides a promising new target for treating neurodegenerative diseases, which currently lack effective disease-modifying therapies.
edited by Lisa Lock , reviewed by Robert Egan
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Add to Preferred Sources Almost complete absence of Psynuclein staining in injected right superior colliculus region vs. noninjected left (outlined and labeled in yellow). Credit: Proceedings of the National Academy of Sciences (2026). DOI: 10.1073/pnas.2622262123 Parkinson's disease is the second most common neurodegenerative disease. Over the last 30 years, studies have shown that a protein called alpha-synuclein abnormally aggregates in people with Parkinson's disease, becoming toxic to neurons in a region of the brain that controls movement. This leads to tremor, rigidity and slowness of movement.
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