Parkinson’s disease is a
neurodegenerative disease that affects people mostly over the age of 65.
Chances of incidence continue to increase in developed countries due to
increased life expectancy and rapid medical advancements. The disease continues
to worsen over time and the cause of it is currently unknown, although there
are many promising leads. It is well known that the brain’s dopamine producing
cells are greatly diminished in those with PD and more correlations are being
discovered to be linked to onset of the disease.
Quite recently, the role of mitochondria
dysfunction has been linked to PD patients. It has been found that there is a
substantial decrease in the activity of mitochondrial NADH ubiquinone
reductase, which is complex I in the ETC. This inevitably results in issues
with the electrochemical gradient across the mitochondrial membrane that aids
in creating ATP, which we know is essential for all bodily functions. Genetics
has also been playing a huge role in Parkinson’s research, as familial form of
PD further point to the role of mitochondrial mutations and dysfunctions. The endoplasmic
reticulum has also been heavily linked to PD and is responsible for production,
delivery and degradation of proteins, notably Lewy bodies. Lewy bodies reflect
the decline of proteostatic competence that accompanies normal aging, which is
a huge factor in inducing Parkinson’s disease. There are also suggestions that
Ca2+ plays a substantial role in onset of Parkinson’s disease and reducing
the influx of Ca2+ should potentially slow triggering symptoms of Parkinson’s
and slow its progression all together. All of these aspects linked to Parkinson’s
are merely strong correlations. Even today, with advancements of medical
technologies, the exact cause of the PD is unknown. The studies done on the
involvement of mitochondrial dysfunction and endoplasmic reticulum are vital in
better understand the molecular and cellular connections in patients with PD
but they do not lead us to a cure.
To help the thousands of
people with PD quickly and efficiently, other than treatment, greater significance
should be placed on preventative measures. The only method that seems most
appropriate in defeating this disease from our population is to find it early, before
any irreversible damage has been done. Jane Brody, in her article “Looking for
Parkinson’s Sooner Years”, describes the various signs to look for before the
onset of PD. Those that eventually succumb to PD “have experienced tremor,
balance problems, constipation, low blood pressure, dizziness, erectile and
urinary dysfunction, fatigue, depression and anxiety” years before the classic
symptoms such as rigidity and tremors.
In addition to those predictive signs, Brody’s
article states that “REM sleep behavior disorder, characterized by a tendency
to act out one’s dreams while asleep, is one of the strongest prediagnostic
symptoms, along with a lost sense of smell and subtle changes in cognition.” This
sleep disorder could affect thousands of people every year who eventually get
diagnosed with PD. The first step in preventing the onset of PD is to
acknowledge these underlying disorders that are strongly correlated with the disease.
Brody mentions that up to eighty percent of those who have REM sleep behavior
disorder get Parkinson’s or other neurodegenerative diseases. As soon as
similar symptoms are observed, patients should consult with a neuro specialist
to learn ways to prevent and delay degeneration while the brain is still mostly
intact.Now that there are prediagnostic symptoms to
look for that are quite common in the population, biomarkers are being studied
to help identify likely PD patients. “Substances in the blood, saliva or cerebrospinal fluid or
imaging characteristics” are the next step in preventing PD in those that are
extremely high risk, as noted in the symptoms that occur years before the severe
degeneration occurs.
Work 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.
Brody, Jane E. “Looking for Parkinson’s Sooner.” Editorial. Nytimes.com.
N.p., 15 Mar. 2015. Web. 19 Oct. 2016. <http://well.blogs.nytimes.com/2015/03/16/looking-for-parkinsons-sooner/>
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