Mitochondrial Mechanisms in Parkinson's Disease Research Paper by Torie

Mitochondrial Mechanisms in Parkinson's Disease
A research paper describing Parkinson's disease as well as the advances made to date in determining potential mitochondrial malfunctions leading to the disease.
# 119666 | 3,325 words | 17 sources | APA | 2010 | US

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This paper delves deeply into the subject of Parkinson's disease, a progressive neurodegenerative disorder, explaining that advances have been made in identifying the genes and environmental factors that may predispose an individual to developing Parkinson's, as well as in developing pharmaceuticals to alleviate some of the physical symptoms of the condition. The paper points out that, regardless, much debate remains over the molecular mechanisms that malfunction and lead to dopaminergic neuron death, the hallmark pathology of Parkinson's. The paper contains various figures of illustration, and concludes that impairment of calcium signaling might lead to protein aggregation as well, and combined with oxidative damage from other sources, might be a key to the selectivity of dopaminergic cell death in Parkinson's disease.

Introduction to Parkinson's Disease
Mitochondrial Function, Malfunction, and Parkinson's Disease
Mitochondria and Parkinson's Disease Genetics: PINK1 and Parkin
Why Dopaminergic Cells?
Proposal for Further Study

From the Paper:

"Although mitochondrial damage has been strongly implicated as a pathway common to idiopathic and familial Parkinson's disease, the question remains as to why dopaminergic neurons are exclusively destroyed. This is especially puzzling considering that mitochondria are universally present in every cell, and both PINK1 and parkin are expressed throughout the brain. One proposed explanation as to why dopaminergic neurons are selectively killed focuses on dopamine metabolism. Within dopaminergic neurons and astrocytes, cytosolic dopamine is hydrolyzed by MAO (monoamine oxidase) into DOPAC (3,4-dihydroxyphenylacetic acid). This process results in the production of free radicals, toxic quinonic compounds and melanin [6]. In addition, dopaminergic neurons are very energy-demanding and may produce more reactive oxygen species by-products of electron transport than other cell types. Placing a population of neurons that is already experiencing stress from natural metabolic processes under even more oxidative stress via mitochondrial damage may be the key as to why dopaminergic neurons are selectively destroyed in Parkinson's disease."

Sample of Sources Used:

  • Bertram L. and Tanzi R.L. Genetics of Neurodegenerative Diseases. In: Siegel, G.J., et al., ed. (2006). Basic Neurochemistry: Molecular, Cellular, and Medical Aspects, 7th ed. (653-666). New York: Elsevier.
  • Blum D., Torch S., Lambeng N., et al. (2001). Molecular pathways involved in the neurotoxicity of 6-OHDA, dopamine and MPTP: contribution to the apoptotic theory in Parkinson's disease. Progress in Neurobiology, Vol 65, 135-172.
  • Cherra, S.J., Dagda R.K., Chu C.T. (2010). Review: Autophagy and neurodegeneration: survival at a cost? Neuropathology and Applied Neurology, Vol 36, 125-132.
  • Dagda R.K. and Chu C.T. (2009). Mitochondrial quality control: insights on how Parkinson's disease related genes PINK1, parkin, and Omi/HtrA2 interact to maintain mitochondrial homeostasis. Journal of Bioenergetics and Biomembranes, Vol 41, 473-479.
  • Dawson T.M. and Dawson V.L. (2003) Molecular Pathways of Neurodegeneration in Parkinson's Disease. Science, Vol 302, 819-822.

Cite this Research Paper:

APA Format

Mitochondrial Mechanisms in Parkinson's Disease (2010, May 16) Retrieved September 24, 2023, from

MLA Format

"Mitochondrial Mechanisms in Parkinson's Disease" 16 May 2010. Web. 24 September. 2023. <>