Running head: PARKINSON’S DISEASE 1

Behind the Chemistry of Parkinson’s Disease

Megan E Quinn

Salt Lake Community College

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Behind the Chemistry of Parkinson’s Disease

Parkinson’s disease is a neurodegenerative disease that affects more than a million people

in the United States of America. It is the second most common neurodegenerative disease

coming next to Alzheimer’s disease. Parkinson’s Disease got its name from a physician named

James Parkinson when he observed and studied six persons who struggled with an unknown

disease in 1817. He created an essay on shaking palsy that eventually gave Parkinson’s Disease

its name. There are four symptoms that are centered around Parkinson’s Disease are

bradykinesia, rigidity, resting tremor, and postural instability. Symptoms in a person with two of

the first three will usually result in a diagnosis of Parkinson’s Disease (Carranza, pg. 1-5).

There have been ten dopaminergic neuronal groups relating to Parkinson’s Disease. In an

article by Viaratis called “Biochemistry of Parkinson’s Disease” it says, “Ten dopaminergic

neuronal groups have been recognized. They are classified as groups A8 to A17. The cell

aggregations (A8, A9, and A10) are in mesencephalon. The cell aggregations (A11, A12, A13,

and A14) are in the diencephalon. A single group of dopaminergic neurons (A15) has been found

in the hypothalamus. A single group of dopaminergic neurons (A16) has been found in the

olfactory bulb. A single group of dopaminergic neurons (A17) has been found in the retina”. The

chemical equation of Parkinson’s Disease is L-tyrosine to L-dopa to Dopamine or also

recognized as “L-Tyrosine + THFA + O2 + Fe2+ + L-Dopa + DHFA + H2O + Fe2+”. The

enzymes that are directly involved with Parkinson’s Disease are L-Tyrosine, TFHA, Pyridoxal

phosphate, and NADH.

Dopamine plays a major role in Parkinson’s Disease as the main transmitter. Dopamine is

created in the substantia nigra by neurons and are transported to striatum using the nigrostriatal
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pathway. Parkinson’s Disease is caused by degeneration of dopamine neurons in the central

nervous system. A person needs a certain amount of dopamine to function properly in the

extrapyramidal system. In order to be diagnosed or even to start showing symptoms of

Parkinson’s Disease there needs to be about 50% striatal dopamine loss. However, there are no

answers to where Parkinson’s Disease comes from and there is not an immediate cure to defeat

the disease only improve quality of life (Carranza, 3).

Within Parkinson’s Disease there are bradykinesia and hypokinesia. Bradykinesia means

slow movements and hypokinesia means the diminished amplitude of movements (Luca, 2). The

bradykinesia is activated with the loss of dopamine that occurs mostly in the putamen, but

responds positively to dopaminergic replacement. Physical signs of bradykinesia and

hypokinesia are loss of functions in fine motor skills and tasks correlated with them. In some

cases a person’s arm will shake or a person make not be able to lift up their foot. Most times it is

described as feeling weak. However, Parkinson’s Disease has no correlation of muscle weakness

or any manual strength. A person with Parkinson’s Disease cannot create movement fast enough

to complete a task and feel like the slow movement is from muscle weakness (Luca, 3).

Parkinson’s Disease has many symptoms that are unpredictable and vary within each

patient. There is currently no way to determine what kind of symptoms someone diagnosed with

Parkinson’s Disease will get but there has been constant data that supports Parkinson’s Disease

symptoms will worsen with age and level of disease severity (Pahwa, 9). The reason for the

correlation between age and increased symptoms has been shown as dopamine start to decrease
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with time then other neurotransmitters may start to interfere and become involved leading to

more symptoms that are different from the degenerating symptoms.

In most cases, Parkinson’s Disease occurs in sixty year old’s and older and rarely occurs

in ages under forty. However, at the beginning of the recorded period the odd of Parkinson’s

Disease is one in two hundred but by the end of the decade the chances increase to one in every

forty people. With this data it concludes that every year there are more diagnoses of Parkinson’s

Disease. Not only is Parkinson’s Disease increasing but the mortality rate is increasing along

with it. There is no data to support that Parkinson’s Disease occurs more in a certain sex.

Parkinson’s Disease has 1.5 to 2.3 time higher mortality record than people without Parkinson’s

Disease (Pahwa, 1).

James Parkinson was a neurologist who wrote an essay called “An Essay on the Shaking

Palsy” where he observed six patients (only actually working with three in person). He became

interested in pursuing medicine at a young age by his father who was a surgeon in his town.

When his father died in 1794 Parkinson took over his father’s practice and became interested in a

variety of different subjects related to science. He became interested in shaking palsy where he

noticed shaking in the hands and legs. That is where he recorded his findings in “An Essay on

the Shaking Palsy” (Carranza, 4). Although he did not only credit himself but gave recognition to

ancient authors who had noticed symptoms of Parkinson’s Disease by shaking limbs. Parkinson

recognized two types of tremors: the action tremor and the involuntary tremor. Parkinson thought

the action tremor was because of lack of motivational force and the involuntary tremor was

because of irregular supply of animal spirits through the nerves (Carranza, 2).
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There has been modern application to Parkinson’s Disease that are working on new

technologies to find a cure or at least find ways for better quality of life. Researchers are

studying the metabolic pathways and looking into genetic mutations that may be factors in

Parkinson’s Disease. Looking into genes they have found mutations in the SNCA gene which

has created evidence to prove that there are rare genetic forms of disease.
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References

Carranza, M. (2013). Parkinson’s Disease : A Guide to Medical Treatment (Vol. First edition). Torino, Italy:

SEEd. Retrieved from

https://libprox1.slcc.edu/login?url=http://search.ebscohost.com/login.aspx?direct=true&db=nlebk&

AN=783067&site=eds-live

Luca Marsili, Giovanni Rizzo, & Carlo Colosimo. (2018). Diagnostic Criteria for Parkinson’s Disease: From

James Parkinson to the Concept of Prodromal Disease. Frontiers in Neurology, Vol 9 (2018).

https://doi-org.libprox1.slcc.edu/10.3389/fneur.2018.00156/full

Parkinson's Disease Brain Chemistry and Effect of Medicines. (n.d.). Retrieved from

http://pdring.com/parkinsons-diseases-brain-chemistry-and-effect-of-medicines.htm

Pahwa, R., & Simuni, T. (2009). Parkinson’s Disease. Oxford: Oxford University Press.

V. (n.d.). Biochemistry of Parkinson's Disease. Retrieved from

http://viartis.net/parkinsons.disease/biochemistry.htm