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Identification of M...
Identification of Multiple QTLs Linked to Neuropathology in the Engrailed-1 Heterozygous Mouse Model of Parkinson's Disease
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- Kurowska, Zuzanna (author)
- Lund University,Lunds universitet,Translationell Neurogenetik,Forskargrupper vid Lunds universitet,Translational Neurogenetics,Lund University Research Groups,Cleveland Clinic Foundation
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- Jewett, Michael (author)
- Lund University,Lunds universitet,Translationell Neurogenetik,Forskargrupper vid Lunds universitet,Translational Neurogenetics,Lund University Research Groups
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- Brattås, Per Ludvik (author)
- Lund University,Lunds universitet,Translationell Neurogenetik,Forskargrupper vid Lunds universitet,Translational Neurogenetics,Lund University Research Groups
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- Jimenez, Itzia (author)
- Lund University,Lunds universitet,Translationell Neurogenetik,Forskargrupper vid Lunds universitet,Translational Neurogenetics,Lund University Research Groups
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- Kenez, Xuyian (author)
- Lund University
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- Björklund, Tomas (author)
- Lund University,Lunds universitet,Molekylär neuromodulering,Forskargrupper vid Lunds universitet,Molecular Neuromodulation,Lund University Research Groups
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- Nordström, Ulrika (author)
- Umeå University,Umeå universitet,Klinisk neurovetenskap
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- Brundin, Patrik (author)
- Van Andel Research Institute
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- Swanberg, Maria (author)
- Lund University,Lunds universitet,Translationell Neurogenetik,Forskargrupper vid Lunds universitet,Translational Neurogenetics,Lund University Research Groups
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(creator_code:org_t)
- 2016-08-23
- 2016
- English.
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In: Scientific Reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 6
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Abstract
Subject headings
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- Motor symptoms in Parkinson's disease are attributed to degeneration of midbrain dopaminergic neurons (DNs). Heterozygosity for Engrailed-1 (En1), one of the key factors for programming and maintenance of DNs, results in a parkinsonian phenotype featuring progressive degeneration of DNs in substantia nigra pars compacta (SNpc), decreased striatal dopamine levels and swellings of nigro-striatal axons in the SwissOF1-En1+/- mouse strain. In contrast, C57Bl/6-En1+/- mice do not display this neurodegenerative phenotype, suggesting that susceptibility to En1 heterozygosity is genetically regulated. Our goal was to identify quantitative trait loci (QTLs) that regulate the susceptibility to PD-like neurodegenerative changes in response to loss of one En1 allele. We intercrossed SwissOF1-En1+/- and C57Bl/6 mice to obtain F2 mice with mixed genomes and analyzed number of DNs in SNpc and striatal axonal swellings in 120 F2-En1+/- 17 week-old male mice. Linkage analyses revealed 8 QTLs linked to number of DNs (p = 2.4e-09, variance explained = 74%), 7 QTLs linked to load of axonal swellings (p = 1.7e-12, variance explained = 80%) and 8 QTLs linked to size of axonal swellings (p = 7.0e-11, variance explained = 74%). These loci should be of prime interest for studies of susceptibility to Parkinson's disease-like damage in rodent disease models and considered in clinical association studies in PD.
Subject headings
- MEDICIN OCH HÄLSOVETENSKAP -- Medicinska och farmaceutiska grundvetenskaper -- Neurovetenskaper (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Basic Medicine -- Neurosciences (hsv//eng)
Publication and Content Type
- ref (subject category)
- art (subject category)
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