Immune protein a possible target to slow Parkinson’s disease
Researchers at Penn Medicine have found that blocking a key neuronal protein interrupts the spread of toxins to healthy neurons in preclinical studies.
1 min. read
Monoclonal antibodies can block a key immune‑related protein that drives the spread of brain cell damage in Parkinson’s disease (PD). This protein, called glycoprotein nonmetastatic melanoma B (GPNMB), may be part of a promising strategy for developing a treatment that slows disease progression at its earliest stages, according to a new study published in Neuronfrom researchers at the Perelman School of Medicine.
The progression of Parkinson’s disease is driven by abnormal clumps of a neuronal protein called alpha‑synuclein. These clumps accumulate inside affected neurons, contributing to their dysfunction and death, and are then released and taken up by nearby healthy neurons. As this pathology moves through different brain regions, patients experience the worsening symptoms that characterize PD.
In preclinical experiments using cultured neurons, antibodies that block GPNMB prevented the spread of alpha‑synuclein pathology from cell to cell.
“These results suggest Parkinson’s disease may be driven by a self reinforcing cycle—alpha-synuclein accumulates in neurons, damaging the neurons. The injury to the neurons initiates the release of GPNMB, which accelerates the spread of alpha-synuclein, leading to further damage,” says lead author Alice Chen‑Plotkin,the Parker Family Professor of Neurology. “Interrupting this cycle would hopefully slow, or even stop, the spread of alpha-synuclein through the brain and the neurodegeneration that follows.”
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