Annotated Bibliography – Parkinson's

Alcalay RN, Caccappolo E, Mejia-Santana H, and et al. “Frequency of Known Mutations in Early-Onset Parkinson Disease: Implication for Genetic Counseling: The Consortium on Risk for Early Onset Parkinson Disease Study.” Archives of Neurology 67, no. 9 (September 1, 2010): 1116–22. doi:10.1001/archneurol.2010.194.

This study was conducted in order to determine the incidence of mutation in 6 commonly known genes associated with Parkinson’s disease. They then used their data to approach genetic counseling and assessment of risk factors for developing familial Parkinson’s disease.


“Alpha-Synuclein and Parkinson’s Disease | The Michael J. Fox Foundation.” Accessed April 18, 2014.

This webpage gives some more basic information between the relationship between alpha-synuclein and how it composes the Lewy bodies which are the signature pathology of Parkinson’s disease. This site is geared towards non-scientific audiences.


Batelli, Sara, Diego Albani, Raffaela Rametta, Letizia Polito, Francesca Prato, Marzia Pesaresi, Alessandro Negro, and Gianluigi Forloni. “DJ-1 Modulates Α-Synuclein Aggregation State in a Cellular Model of Oxidative Stress: Relevance for Parkinson’s Disease and Involvement of HSP70.” Edited by Hilal Lashuel. PLoS ONE 3, no. 4 (April 2, 2008): e1884.

This article illustrates the role of DJ-1 and it’s role in alpha-synuclein aggregation and the role of HSP70 in the death of dopaminergic cells.


Brooks, D. J. “Dopamine Agonists: Their Role in the Treatment of Parkinson’s Disease.” Journal of Neurology, Neurosurgery & Psychiatry 68, no. 6 (June 1, 2000): 685–89. doi:10.1136/jnnp.68.6.685.

This article discusses the method by which dopamine agonists work to help treat the effects of Parkinson’s disease.


Conway, Kelly A., Seung-Jae Lee, Jean-Christophe Rochet, Tomas T. Ding, Robin E. Williamson, and Peter T. Lansbury. “Acceleration of Oligomerization, Not Fibrillization, Is a Shared Property of Both Α-Synuclein Mutations Linked to Early-Onset Parkinson’s Disease: Implications for Pathogenesis and Therapy.” Proceedings of the National Academy of Sciences 97, no. 2 (January 18, 2000): 571–76. doi:10.1073/pnas.97.2.571.

This paper shows how the alpha-synuclein affects the substantia nigra and that it is the oligomerization of the alpha-synuclein, not the fibrillization is what causes the pathology found in Parkinson’s disease.


“Diagnosis.” University of Maryland Medical Center. Accessed May 9, 2014.

This site outlines how Parkinson’s is diagnosed and explains why a conclusive diagnosed can’t be confirmed. Instead, physicians take into account the symptoms, medical history, etc to determine clinically that a patient is suffering from Parkinson’s rather than something that can present with similar symptoms.


“Dr James Parkinson.” Accessed May 8, 2014.

This is a historical page on Dr. James Parkinson and his discovery/description of Parkinson’s for the first time. It also gives his original essay on “Shaky Palsy.”


Espinoza, Stefano, Francesca Manago, Damiana Leo, Tatyana D Sotnikova, and Raul R Gainetdinov. “Role of Catechol-O-Methyltransferase (COMT)-Dependent Processes in Parkinson’s Disease and L-DOPA Treatment.” CNS & Neurological Disorders Drug Targets 11, no. 3 (May 2012): 251–63.

This paper examined the role of catechol-O-methyltransferase (COMT) activity and the role it plays in the degradation of dopamine and norepinephrine, both in the periphery and the central nervous system. They were looking for a connection between COMTs and the dopamine degradation involved in Parkinson’s disease.


Ferretta, Anna, Antonio Gaballo, Paola Tanzarella, Claudia Piccoli, Nazzareno Capitanio, Beatrice Nico, Tiziana Annese, et al. “Effect of Resveratrol on Mitochondrial Function: Implications in Parkin-Associated Familiar Parkinson’s Disease.” Biochimica et Biophysica Acta (BBA) – Molecular Basis of Disease 1842, no. 7 (July 2014): 902–15. doi:10.1016/j.bbadis.2014.02.010.

This paper shows the effects resveratrol, a polyphenolic compound, has on the regulation of mitchondrial processes and function. They are able to show that resveratrol regulates energy homeostasis through activation of AMP-kinases and SIRT1 to handle increases oxidative stress from Parkinson’s disease.


Gage, Fred H., and Sally Temple. “Neural Stem Cells: Generating and Regenerating the Brain.” Neuron 80, no. 3 (October 30, 2013): 588–601. doi:10.1016/j.neuron.2013.10.037.

Novel study into neural cell regeneration in a mouse model, implications for potential human applications for regeneration of depleted dopaminergic cells.


Hughes, A J, S E Daniel, L Kilford, and A J Lees. “Accuracy of Clinical Diagnosis of Idiopathic Parkinson’s Disease: A Clinico-Pathological Study of 100 Cases.” Journal of Neurology, Neurosurgery, and Psychiatry 55, no. 3 (March 1992): 181–84.

This paper discussed how the diagnosis of Parkinson’s disease is deduced and what factors are required. Since Parkinson’s can be caused by many factors, diagnoses are not always accurate.


Jankovic, J. “Parkinson’s Disease: Clinical Features and Diagnosis.” Journal of Neurology, Neurosurgery & Psychiatry 79, no. 4 (April 1, 2008): 368–76. doi:10.1136/jnnp.2007.131045.

This paper indicates ways to diagnose Parkinson’s disease in the clinic by identifying common signs and symptoms of the disease and how to differentiate Parkinson’s from other diseases with some of the same symptoms.


Kim, Mia, Ki-Ho Cho, Mal-Soon Shin, Jae-Min Lee, Han-Sam Cho, Chang-Ju Kim, Dong-Hoon Shin, and Hyeon Yang. “Berberine Prevents Nigrostriatal Dopaminergic Neuronal Loss and Suppresses Hippocampal Apoptosis in Mice with Parkinson’s Disease.” International Journal of Molecular Medicine, February 13, 2014. doi:10.3892/ijmm.2014.1656.

This article illustrates a mouse model of how the dopaminergic neurons in patients with Parkinson’s disease might be spared from apoptosis with the use of a compound, berberine, isolated from a natural plant.


Lee, A K. “Dopamine (D2) Receptor Regulation of Intracellular Calcium and Membrane Capacitance Changes in Rat Melanotrophs.” The Journal of Physiology 495, no. Pt 3 (September 15, 1996): 627–40.

This study shows the role the dopamine D2 receptor plays on intracellular calcium levels in a rat melanotroph. This demonstrates how the D2 receptor is involved in movement, which is affected by Parkinson’s.


Marder KS, Tang MX, Mejia-Santana H, and et al. “Predictors of Parkin Mutations in Early-Onset Parkinson Disease: The Consortium on Risk for Early-Onset Parkinson Disease Study.” Archives of Neurology 67, no. 6 (June 1, 2010):731–38. doi:10.1001/archneurol.2010.95.

This study was aimed at determining indications in Parkin genes as a way to assess the likelihood of a patient developing early-onset Parkinson’s disease.


Missale, Cristina, S. Russel Nash, Susan W. Robinson, Mohamed Jaber, and Marc G. Caron. “Dopamine Receptors: From Structure to Function.” Physiological Reviews 78, no. 1 (January 1, 1998): 189–225.

This article describes the structure and function of the family of dopamine receptors and how they trigger signal transduction pathways in the cell.


“Nature 2013 501 512_Parkin.pdf.”  

This paper shows the role of Parkin and how it is used in the macrophagy of intracellular pathogens. It is one of the proteins involved in locating pathogens and shuttling them into the pathways that break them down before they cause damage to the cell.


Oczkowska, Anna, Margarita Lianeri, Wojciech Kozubski, and Jolanta Dorszewsk. “Mutations of PARK Genes and Alpha-Synuclein and Parkin Concentrations in Parkinson’s Disease.” In A Synopsis of Parkinson’s Disease, edited by Abdul Qayyum Rana MdFrcpc Frcp – Uk hon. InTech, 2014.

This paper tested the effects of known gene mutations involved in the development of Parkinson’s disease and their downstream effects on levels of plasma Parkin and glycosylated form of alpha-synuclein.


Padmaja, M. Vishwanathan, Meenakshi Jayaraman, Avathvadi Venkatesan Srinivasan, C. R. Srikumari Srisailapathy, and Arabandi Ramesh. “PARK2 Gene Mutations in Early Onset Parkinson’s Disease Patients of South India.” Neuroscience Letters 523, no. 2 (August 15, 2012): 145–47. doi:10.1016/j.neulet.2012.06.062.

This team analyzed the coding exons of the PARK2 gene to determine the incidence of mutation to specific exons of the gene in Parkinson’s patients.


Pan, Tianhong, Seiji Kondo, Weidong Le, and Joseph Jankovic. “The Role of Autophagy-Lysosome Pathway in Neurodegeneration Associated with Parkinson’s Disease.” Brain 131, no. 8 (August 1, 2008): 1969–78. doi:10.1093/brain/awm318.

This paper looked at the role of the autophagy-lysosome pathway (ALP) as a possible cause for the accumulation of non-mutant alpha-synuclein proteins in dopaminergic cells in the brain. Since the build up of alpha-synuclein causes the Lewy bodies, dysfunction of the ALP may be a possible contributor to Parkinson’s disease.


“Parkinson Disease,” April 17, 2014.

This site describes the symptoms, incidence, genetic factors, and inheritance of Parkinson’s disease for a non-scientific audience. It also provides links for further information about the disease.


“Parkinson’s Symptoms.” Accessed May 8, 2014.

Description of common and potential signs and symptoms of Parkinson’s disease.


Polymeropoulos, Mihael H., Christian Lavedan, Elisabeth Leroy, Susan E. Ide, Anindya Dehejia, Amalia Dutra, Brian Pike, et al. “Mutation in the Α-Synuclein Gene Identified in Families with Parkinson’s Disease.” Science 276, no. 5321 (June 27, 1997): 2045–47. doi:10.1126/science.276.5321.2045.

This article in Science isolated specific mutations in the alpha-synuclein gene that promote a familial inheritance of Parkinson’s disease mutations.


Ren, Jie, Yuanyuan Zhang, Huizi Jin, Jing Yu, Yueyang Zhou, Fang Wu, and Weidong Zhang. “Novel Inhibitors of Human DOPA Decarboxylase Extracted from Euonymus Glabra Roxb.” ACS Chemical Biology 9, no. 4 (April 18, 2014): 897–903. doi:10.1021/cb500009r

Discovery of a new compound found naturally in a species of plant capable of selecting for DOPA decarboxylase instead of a generalized decarboxylase inhibitor.


Schapira, Anthony H. V. “Etiology of Parkinson’s Disease.” Neurology 66, no. 10 suppl 4 (May 23, 2006): S10–S23. doi:10.1212/WNL.66.10_suppl_4.S10.

This paper ends the ambiguity of from where Parkinson’s was thought to originate. Until this paper, Parkinson’s causes hadn’t been conclusively, but this paper locates mutations in alpha-synuclein, parkin, UCHL1, DJ1, PINK1, and LRRK2 as direct causes to PD. Furthermore, they find these mutations to follow a Mendelian pattern of inheritance.


“The Synaptic Pathology of Α-Synuclein Aggregation in Dementia with Lewy Bodies, Parkinson’s Disease and Parkinson’s Disease Dementia – Springer.” Accessed April 18, 2014.

This paper details the role the alpha-synuclein aggregates found in Parkinson’s patients cause dysfunction and eventual degeneration of neurons.


Tao, Xiao, and Liang Tong. “Crystal Structure of Human DJ-1, a Protein Associated with Early Onset Parkinson’s Disease.” Journal of Biological Chemistry 278, no. 33 (August 15, 2003): 31372–79. doi:10.1074/jbc.M304221200.

This article solves the crystal structure of DJ-1, a protein that had previously been linked to early-onset of Parkinson’s disease. This is the first crystal structure of this protein and was solved at 1.8ª resolution.


Valente, Enza Maria, Patrick M. Abou-Sleiman, Viviana Caputo, Miratul M. K. Muqit, Kirsten Harvey, Suzana Gispert, Zeeshan Ali, et al. “Hereditary Early-Onset Parkinson’s Disease Caused by Mutations in PINK1.” Science 304, no. 5674 (May 21, 2004): 1158–60. doi:10.1126/science.1096284.

This paper illustrates common mutations to PINK1 that are associated with PARK6 and their roles in Parkinson’s disease. The data shows the link between mitochondria and pathogenesis of Parkinson’s disease on a molecular level.


Wu, Feng, Zhong Wang, Jin-Hua Gu, Jian-Bin Ge, Zhong-Qin Liang, and Zheng-Hong Qin. “p38(MAPK)/p53-Mediated Bax Induction Contributes to Neurons Degeneration in Rotenone-Induced Cellular and Rat Models of Parkinson’s Disease.” Neurochemistry International 63, no. 3 (September 2013): 133–40. doi:10.1016/j.neuint.2013.05.006.

Rotenone is a known neurtoxin that causes degeneration of dopamingergic cells, such as those in the substantia nigra. This is what happens in Parkinson’s disease so this team studied how rotenone affected some of the cell’s natural defenses from apoptosis, p38MAPK and p53.

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