New Study Reveals Target for Treating Movement Disorders
Researchers at Vanderbilt University have reported that blocking a nerve-cell receptor in brain that coordinates movement could improve movement disorders.
The findings of the study was published in the journal Neuron on January 18, 2018. The study focuses on M4, a subtype of the muscarinic acetylcholine family of nerve cell neuron receptors activated by binding the neurotransmitter acetylcholine. The Vanderbilt scientists found that M4 neurons project into the substantia nigra pars reticulata, a small structure near the base of the brain important in regulating movement. M4 receptor activation opposes signals another class of receptors that binds the neurotransmitters dopamine.
In Parkinson’s disease, dopamine-producing neurons starts degrading opposing action of M4 neurons can suppress dopamine signaling even further. “M4 muscarinic receptor activation has a much more pivotal role in controlling dopamine signaling than we thought,” said P. Jeffrey Conn, Ph.D., corresponding author of the study. Although drugs that block muscarinic acetylcholine receptors can relieve symptoms of Parkinson’s disease including tremors and muscle rigidity. They also block the whole muscarinic acetylcholine family of receptors, these drugs cause adverse side effects patients. The identification of different subtypes of the muscarinic acetylcholine receptor raised the possibility of selectively targeting treatment in a way that avoids unwanted side effects.
According to Parkinson’s disease Therapeutic Market report published by Coherent Market Insights, Parkinson’s disease (PD) is a chronic disorder characterized by the malfunctioning and death of vital nerve cells in the brain, and can be characterized by tremor, dementia, and depression. Conn and his colleagues have been developing potential drugs called positive allosteric modulators that can boost the activity of the M4 receptor such as the dimmer in an electrical circuit. “We used genetic approaches and now have very selective compounds that have anti-parkinsonian activity in animal models,” said Conn, the Lee E. Limbird Professor of Pharmacology in the School of Medicine.
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