Parkinson's Disease Researcher's Attempt to Find a Definitive Cure

          Johnny Cash, Mohammad Ali, and Michael J. Fox. Other than being insanely talented, what do all three of these people have in common? These famous men, along with ten million others share one thing: Parkinson’s disease. To this day, scientists across the globe attempt to crack the code on this intricate disease.

Parkinson’s disease is long-term neurodegenerative disorder that targets motility. This disease is seen amongst older men and women. Parkinson’s is heavily associated with dopamine. Dopamine neurotransmitters are a major contributor to our reward center as well as our locomotor abilities. Some symptoms of Parkinson’s include rigidity, tremors, and slow movements. It is believed that the cause of Parkinson’s is the death of cells in the substantia nigra – specifically death of dopamine neurotransmitters.

However, in Dr. James Surmeier and his colleague’s article titled Calcium, cellular aging, and selective neuronal vulnerability in Parkinson’s disease it states that this might not actually be the case. There is considerable doubt that the “cellular stress alone” is the cause for the loss of dopamine neurotransmitters in Parkinson’s. Studies now show that there is “regional variability in the vulnerability” of dopamine (pg. 176). Not only this, but when patients received L-DOPA administration – which has the purpose of elevating dopamine levels – their disease did not progress faster. Researchers have also found that other neurons – not just dopamine – have died in Parkinson’s patients. This suggests that dopamine itself is not the primary cause of this neurodegenerative disease.

Surmeier and his fellow researchers believe that Parkinson’s disease is caused due to an excess influx of calcium. In the article it states that “epidemiological data…supports a linkage between L-type Ca²⁺ channels and the risk of developing PD” (pg. 175). Recently, researchers have learned that mitochondrial dysfunction has a role in Parkinson’s. It is found that PD patients have decreased activity in the mitochondrial NADH ubiquinone reductase. This means that patients of this disease face “oxidative damage to complex I” (pg. 175). From this, Surmeier et al. concluded that the oxidative stress is likely to stem from the mitochondria. This article suggests that the cause of PD is an increase of calcium levels which causes rapid aging in the SNc DA neurotransmitters. A possible way to combat this disease could be to figure out a way to reduce the Ca²⁺ levels in the brain. Surmeier proposes that this may be possible through DHP L-type channels. DHP is a calcium channel antagonist. These channels are proven to be safe in humans and therefore, an oral medication can be made. Through human studies, researchers found that certain DHP that surpasses that brain-blood barrier are able to reduce the likelihood of being diagnosed with PD. Through this discovery, they learned that an antagonist that was able to cross the brain-blood barrier and was a powerful Cav1.3 would “be a very effective neuroprotective agent” (pg. 178). This shows us that there may be hope after all for Parkinson’s disease patients.

In Carl Zimmer’s article tilted Clues to How an Electric Treatment for Parkinson’s Works, we learn that another interesting treatment to Parkinson’s disease is called deep brain stimulation. In the article, Dr. Starr from University of California, San Francisco put electrodes in the brains of Parkinson’s disease patients. After the surgery, Dr. Starr turned on the electrodes which caused a stream of buzzing electric pulses within the brain. His technique was successful as a number of patients felt the effect instantly. According to Dr. Starr when the patients are not taking their medications and are unable to move, suddenly can walk after the stimulation. Dr. Starr points out that although deep brain stimulation work, he does not really know the underlying causes as to why it so successful

To target the disease, neurosurgeons like Dr. Starr places electrodes into the basal ganglia where the dopamine neurotransmitters are usually made. Scientific studies have revealed that Parkinson’s alters the brain’s electrical rhythm. One of the rhythms that are prominently altered is the beta rhythm. The beta rhythm becomes stronger throughout the entire brain in patients with Parkinson’s disease. A significant correlation that Dr. Starr made was that deep brain stimulation causes the cortex to be less synchronized. This reduces the effects of the potent synchrony of the beta rhythm in PD patients that do not receive treatment.

Looking at Mohammad Ali, and others like him that have suffered from this disease, I believe it is safe to say that there is a correlation between the external environment and the molecular chemistry of our brains. With this said, both of these articles offer intriguing evidence of the extremely complex nature of Parkinson’s disease. It is clear that this disease is something that has researcher and doctors still very perplexed. There are a multitude of factors that go into the neurodegenerative disease. The biology is deeply intertwined with a myriad of cellular components which makes targeting the cause of Parkinson’s disease even harder to comprehend. 

Works Cited:
Surmeier, D. James, Jaime N. Guzman, and Javier Sanchez-Padilla. “Calcium, Cellular Aging, and Selective Neuronal Vulnerability in Parkinson’s Disease.”Cell calcium 47.2 (2010): 175–182. PMC. Web. 19 Oct. 2016.
Zimmer, Carl. "Clues to How an Electric Treatment for Parkinson’s Works." The New York Times. The New York Times, 15 Apr. 2015. Web. 19 Oct. 2016.