Dopamine loss is what leads to the motor and non motor symptoms of Parkinson’s. How do we prevent or fight against it? New research may have found a possible answer through a receptor called GUCY2, or Guanylyl cyclase C.
Researchers believe that the loss of dopamine is partly due to the dysfunction of mitochondria. Most of us can think back to grade school science where we learned that the mitochondria is the powerhouse of the cell. The mitochondria is what helps produce energy for our body systems.
Guanylyl cyclase C (GUCY2C) is a receptor that lies on the surface of the dopamine neurons and in the part of the brain that produced dopamine, the substantia nigra. A recent study by Scott Waldman provided clues on how GUCY2C can be used as protection against the dopamine death and mitochondrial dysregulation.
The study involved two groups of mice, one with the GUCY2C receptor and one without. Both groups were given a toxin that produced PD symptoms, and the study examined how GUCY2C played a role in neuroprotective mechanisms. The mice that did not have GUCY2C receptors had higher rates of dopamine death. Even more interestingly, the mice that did have GUCY2C receptors showed an increased production in GUCY2C. The authors believe this to be a protective mechanism.
Further protective mechanisms were found via cyclic GMP (cGMP), which is a byproduct of GUCY2C activation. Cyclic GMP is thought to protect dopamine neurons from oxidative stress and mitochondrial dysfunction. This begged a crucial question: can there be a drug that increases cGMP to produce dopamine neurons?
The authors also questioned whether GUCY2C may serve as an early indicator of Parkinson’s. More research is needed before things would move forward, but this is an exciting first step!
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