DOI: http://dx.doi.org/10.18203/2394-6040.ijcmph20204402

A new area of stem cell therapy for Parkinson disease

Khaled M. Hassan, Zahra H. Alqarni, Ali A. Almontashri, Ahmed M. Allubly, Khalid A. Alalmaee, Fatemah A. Alhalawani, Fahad M. Alshalfan, Muayad M. Anbarserri, Mohammed S. Almalki, Mohammed A. Tai, Weaam A. Felemban, Mansoor D. Alhassani, Ali A. Alkhamis, Atheer A. Alsultan, Saud N. Almuqbil, Fahad S. Alsadoon

Abstract


No treatment currently can be used in order to slow or even stop the progression of Parkinson's disease. Nowadays, researchers are already using stem cells to grow dopamine-producing nerve cells in the lab so that they can study the disease, especially in those cases where there is a known genetic cause for the condition. The development of the advanced cellular therapies and using induced pluripotent stem cells is making it possible to combat the progression of the disease without the resulting motor complications. It has been shown that the transplantation of many cell sources leads to reduce Parkinson’s disease symptoms in animal models.


Keywords


Parkinson's disease, Stem cells, Pluripotent stem cells, Alpha synuclein, Animal model, Cell therapy, Dopaminergic neurons, Induced pluripotent stem cells, Neurodegeneration

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References


Satake W, Nakabayashi Y, Mizuta I, Hirota Y, Ito C, Kubo M, et al. Genome-wide association study identifies common variants at four loci as genetic risk factors for Parkinson′s disease. Nat Genet. 2009;41,1303-7.

Simon-Sanchez J, Schulte C, Bras JM, Sharma M, Gibbs JR, Berg D, et al. Genome-wide association study reveals genetic risk underlying Parkinson′s disease. Nat Genet. 2009;41,1308-12.

Bellenguez C, Bevan S, Gschwendtner A, Spencer CC, Burgess AI, Pirinen M, et al. Dissection of the genetics of Parkinson′s disease identifies an additional association 5′ of SNCA and multiple associated haplotypes at 17q21. Hum Mol Genet. 2011;20:345-53.

Kempster PA, O’Sullivan SS, Holton JL, Revesz T, Lees AJ. Relationships between age and late progression of Parkinson′s disease: a clinico-pathological study. Brain. 2010;133:1755-62.

Masliah E, Rockenstein E, Veinbergs I, Mallory M, Hashimoto M, Takeda A, et al. Dopaminergic loss and inclusion body formation in alpha-synuclein mice: implications for neurodegenerative disorders. Science. 287. 2000;1265-69.

Feany MB, Bender WW. A Drosophila model of Parkinson's disease. Natur. 2000;404(6776):394-8.

Dawson TM, Ko HS, Dawson VL. Genetic animal models of Parkinson's disease. Neuro. 2010;66(5): 646-61.

Larsen K, Hedegaard C, Bertelsen MF, Bendixen C. Threonine 53 in α-synuclein is conserved in long-living non-primate animals. Biochemi Biophysic Resear Communicat. 2009;387(3):602-5.

Bottomley RH, Trainer AL, Griffin MJ. Enzymatic and chromosomal characterization of HeLa variants. J Cell Biol. 1969;41(3):806-15.

Jankovic J. Parkinson?s disease: clinical features and diagnosis. J Neurol Neurosurg Psychiatr. 2008;79:368-76.

Devine MJ, Ryten M, Vodicka P, Thomson AJ, Burdon T, Houlden H, et al. Parkinson's disease induced pluripotent stem cells with triplication of the α-synuclein locus. Nature Communications. 2011;2(1):1-0.

Polymeropoulos MH, Lavedan C, Leroy E, Ide SE, Dehejia A, Dutra A, et al. Mutation in the α-synuclein gene identified in families with Parkinson's disease. Science. 1997;27;276(5321): 2045-7.

Spillantini MG, Schmidt ML, Lee VM, Trojanowski JQ, Jakes R, Goedert M. α-Synuclein in Lewy bodies. Nature. 1997;388(6645):839-40.

Singleton AB, Farrer M, Johnson J, Singleton A, Hague S, Kachergus J, et al. [alpha]-synuclein locus triplication causes Parkinson's disease. Science. 2003;302(5646):841-2.

Ibanez P, Bonnet AM, Debarges B, Lohmann E, Tison F, Agid Y, et al. French Parkinson's Disease Genetics Study Group. Causal relation between α-synuclein locus duplication as a cause of familial Parkinson's disease. Lancet. 2004;364(9440):1169-71.