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Viral Vector Mediated Overexpression of Human alpha-Synuclein in the Nigrostriatal Dopaminergic Neurons: A New Model for Parkinson's Disease.

Maingay, Matthew LU ; Romero-Ramos, Marina LU and Kirik, Deniz LU (2005) In CNS Spectrums 10(3). p.235-244
Abstract
Parkinson’s disease is predominantly a dopamine deficiency syndrome, which is produced in the brain by the loss of cells located in a small area in the ventral midbrain called the substantia nigra. Complete unilateral dopamine lesions, based on the administration of toxic substances (ie, 6-hydroxy-dopamine in rats and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in mice and primates) have been extremely useful in testing strategies of replacement. For example, the functional and biochemical impact of the transplanted ventral mesencephalic dopaminergic progenitors has been characterized to a large extent, using the complete lesion model in rats. Over the last decade, however, studies addressing the ability of neurotrophic factors to protect... (More)
Parkinson’s disease is predominantly a dopamine deficiency syndrome, which is produced in the brain by the loss of cells located in a small area in the ventral midbrain called the substantia nigra. Complete unilateral dopamine lesions, based on the administration of toxic substances (ie, 6-hydroxy-dopamine in rats and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in mice and primates) have been extremely useful in testing strategies of replacement. For example, the functional and biochemical impact of the transplanted ventral mesencephalic dopaminergic progenitors has been characterized to a large extent, using the complete lesion model in rats. Over the last decade, however, studies addressing the ability of neurotrophic factors to protect injured dopamine cells prompted researchers to make available partial and progressive lesion models to allow a window of opportunity to interfere the disease progression. Recent findings relating α-synuclein with Parkinson’s disease pathology have opened new possibilities to develop alternative models based on the overexpression of this protein using recombinant adeno-associated viral vectors, which is valuable not only for helping to better understand its involvement in the disease process, but also to more closely resemble the neurodegeneration found in Parkinson’s disease. (Less)
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author
organization
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Contribution to journal
publication status
published
subject
in
CNS Spectrums
volume
10
issue
3
pages
235 - 244
publisher
MBL Communications
external identifiers
  • wos:000228492600022
  • pmid:15744224
ISSN
1092-8529
language
English
LU publication?
yes
id
8dab96ca-c3e6-4f10-9a35-0b31c10be138 (old id 135228)
alternative location
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15744224&dopt=Abstract
http://www.cnsspectrums.com/aspx/articledetail.aspx?articleid=284
date added to LUP
2007-07-17 12:35:35
date last changed
2016-09-30 05:39:15
@article{8dab96ca-c3e6-4f10-9a35-0b31c10be138,
  abstract     = {Parkinson’s disease is predominantly a dopamine deficiency syndrome, which is produced in the brain by the loss of cells located in a small area in the ventral midbrain called the substantia nigra. Complete unilateral dopamine lesions, based on the administration of toxic substances (ie, 6-hydroxy-dopamine in rats and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in mice and primates) have been extremely useful in testing strategies of replacement. For example, the functional and biochemical impact of the transplanted ventral mesencephalic dopaminergic progenitors has been characterized to a large extent, using the complete lesion model in rats. Over the last decade, however, studies addressing the ability of neurotrophic factors to protect injured dopamine cells prompted researchers to make available partial and progressive lesion models to allow a window of opportunity to interfere the disease progression. Recent findings relating α-synuclein with Parkinson’s disease pathology have opened new possibilities to develop alternative models based on the overexpression of this protein using recombinant adeno-associated viral vectors, which is valuable not only for helping to better understand its involvement in the disease process, but also to more closely resemble the neurodegeneration found in Parkinson’s disease.},
  author       = {Maingay, Matthew and Romero-Ramos, Marina and Kirik, Deniz},
  issn         = {1092-8529},
  language     = {eng},
  number       = {3},
  pages        = {235--244},
  publisher    = {MBL Communications},
  series       = {CNS Spectrums},
  title        = {Viral Vector Mediated Overexpression of Human alpha-Synuclein in the Nigrostriatal Dopaminergic Neurons: A New Model for Parkinson's Disease.},
  volume       = {10},
  year         = {2005},
}