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Brain protein overactive in Parkinson’s disease

28 September 2017

A team of neuroscientists led by Joost Verhaagen from the Netherlands Institute for Neuroscience (NIN) demonstrated for the first time that a protein involved in the formation of nerve fibers and neuronal connections could be involved in Parkinson’s disease. The findings have been published in the Journal of Neuroscience. The discovery provides a new perspective for developing a treatment for Parkinson’s disease.

Parkinson’s disease

Parkinson’s disease is a neurodegenerative disease characterized by severe motor dysfunction due to progressive degeneration of dopamine-producing cells in the substantia nigra, a deeper part of the brain. Dopamine is a so-called neurotransmitter, a chemical released by neurons to send signals to other neurons. Low dopamine levels make it difficult to control the muscles, which can lead to muscle stiffness, slow movement and strong tremor. Behavioral and cognitive problems may also occur.


Previous result show that the presence of the protein RGMa is highly increased in the substantia nigra of patients with Parkinson’s disease. Scientists of the NIN, VU University and Brain Center Rudolf Magnus have now expressed the RGMa protein in the dopamine-producing cells in substantia nigra of healthy mice. Overexpression of RGMa induced the degeneration of dopamine-producing cells and this resulted in a progressive movement disorder, including changes in motor coordination and imbalance, similar to the clinical and neuropathological hallmarks of Parkinson’s disease. Verhaagen: “It seems that too much of the RGMa protein in Parkinson’s patients affects the connections between dopamine-producing cells and other nerve cells, consequently causing the death of these cells.”

Further research will have to show whether the neutralization of this protein may be of therapeutic value to Parkinson’s patients.

Publication: Repulsive guidance molecule a (RGMa) induces neuropathological and behavioral changes that closely resemble Parkinson’s disease Journal of Neuroscience


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