RGD Reference Report - Potential role of α-synuclein in neurodegeneration: studies in a rat animal model. - Rat Genome Database

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Potential role of α-synuclein in neurodegeneration: studies in a rat animal model.

Authors: Stoica, George  Lungu, Gina  Bjorklund, Nicole L  Taglialatela, Giulio  Zhang, Xing  Chiu, Veronica  Hill, Herbert H  Schenk, James O  Murray, Ian 
Citation: Stoica G, etal., J Neurochem. 2012 Aug;122(4):812-22. doi: 10.1111/j.1471-4159.2012.07805.x. Epub 2012 Jun 22.
RGD ID: 42722007
Pubmed: PMID:22639889   (View Abstract at PubMed)
DOI: DOI:10.1111/j.1471-4159.2012.07805.x   (Journal Full-text)

Neuronal protein α-synuclein (α-syn) is an essential player in the development of neurodegenerative diseases called synucleinopathies. A spontaneous autosomal recessive rat model for neurodegeneration was developed in our laboratory. These rats demonstrate progressive increases in α-syn in the brain mesencephalon followed by loss of dopaminergic terminals in the basal ganglia (BG) and motor impairments. The severity of pathology is directly related to the overexpression of α-syn and parallel decrease in dopamine (DA) level in the striatum (ST) of affected rats. The neurodegeneration in this model is characterized by the presence of perikarya and neurites Lewis bodies (LB) and diffuse marked accumulation of perikaryal α-syn in the substantia nigra (SN), brain stem (BS), and striatum (ST) along with neuronal loss. Light and ultrastructural analyses revealed that the process of neuronal degeneration is a 'dying back' type. The disease process is accompanied by gliosis and release of inflammatory cytokines. This neurodegeneration is a multisystemic disease and implicate α-syn as a major factor in the pathogenesis of this inherited autosomal recessive animal model. Decrease dopamine (DA) and overexpression of α-syn in the brain mesencephalon may provide a naturally occurring animal model for Parkinson's disease (PD) and other synucleinopathies that reproduces significant pathological, neurochemical, and behavioral features of the human disease.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
synucleinopathy  IAGP 42722007compared to control BD-IVRGD 

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
negative regulation of dopamine secretion  IMP 42722007 RGD 
reactive gliosis  IMP 42722007 RGD 

Phenotype Annotations    Click to see Annotation Detail View

Mammalian Phenotype

TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
abnormal medium spiny neuron morphology  IAGP 42722007compared to control BD-IVRGD 
abnormal olfactory bulb interneuron morphology  IAGP 42722007compared to control BD-IVRGD 
abnormal substantia nigra pars compacta morphology  IAGP 42722007compared to control BD-IVRGD 
alpha-synuclein inclusion body  IAGP 42722007compared to control BDIVRGD 
astrocytosis  IAGP 42722007compared to control BD-IVRGD 
increased interleukin-1 beta secretion  IAGP 42722007compared to control BD-IVRGD 
microgliosis  IAGP 42722007compared to control BD-IVRGD 
neuron degeneration  IAGP 42722007compared to control BD-IVRGD 
Objects Annotated

Genes (Rattus norvegicus)
Myo5a  (myosin VA)

BDIV-Myo5a/StcRrrc  (NA)

Additional Information