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Human α-synuclein o...
Human α-synuclein overexpression in a mouse model of Parkinson’s disease leads to vascular pathology, blood brain barrier leakage and pericyte activation
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- Elabi, Osama (författare)
- Lund University,Lunds universitet,Translationell Neurologi,Forskargrupper vid Lunds universitet,WCMM- Wallenberg center för molekylär medicinsk forskning,Medicinska fakulteten,Translational Neurology (TNY),Lund University Research Groups,WCMM-Wallenberg Centre for Molecular Medicine,Faculty of Medicine
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- Gaceb, Abderahim (författare)
- Lund University,Lunds universitet,Translationell Neurologi,Forskargrupper vid Lunds universitet,WCMM- Wallenberg center för molekylär medicinsk forskning,Medicinska fakulteten,Translational Neurology (TNY),Lund University Research Groups,WCMM-Wallenberg Centre for Molecular Medicine,Faculty of Medicine
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- Carlsson, Robert (författare)
- Lund University,Lunds universitet,Translationell Neurologi,Forskargrupper vid Lunds universitet,WCMM- Wallenberg center för molekylär medicinsk forskning,Medicinska fakulteten,Translational Neurology (TNY),Lund University Research Groups,WCMM-Wallenberg Centre for Molecular Medicine,Faculty of Medicine
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- Padel, Thomas (författare)
- Lund University,Lunds universitet,Translationell Neurologi,Forskargrupper vid Lunds universitet,WCMM- Wallenberg center för molekylär medicinsk forskning,Medicinska fakulteten,Translational Neurology (TNY),Lund University Research Groups,WCMM-Wallenberg Centre for Molecular Medicine,Faculty of Medicine
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- Soylu-Kucharz, Rana (författare)
- Lund University,Lunds universitet,Biomarkörer vid hjärnsjukdomar,Forskargrupper vid Lunds universitet,Wallenberg Neurocentrum, Lund,Medicinska fakulteten,Biomarkers in Brain Disease,Lund University Research Groups,Wallenberg Neuroscience Centre, Lund,Faculty of Medicine
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- Cortijo, Irene (författare)
- Lund University
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- Li, Wen (författare)
- Lund University,Lunds universitet,Neural plasticitet och reparation,Forskargrupper vid Lunds universitet,Wallenberg Neurocentrum, Lund,Medicinska fakulteten,Neural Plasticity and Repair,Lund University Research Groups,Wallenberg Neuroscience Centre, Lund,Faculty of Medicine
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- Li, Jia Yi (författare)
- Lund University,Lunds universitet,Neural plasticitet och reparation,Forskargrupper vid Lunds universitet,Wallenberg Neurocentrum, Lund,Medicinska fakulteten,Neural Plasticity and Repair,Lund University Research Groups,Wallenberg Neuroscience Centre, Lund,Faculty of Medicine,China Medical University, Shenyang
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- Paul, Gesine (författare)
- Lund University,Lunds universitet,Translationell Neurologi,Forskargrupper vid Lunds universitet,WCMM- Wallenberg center för molekylär medicinsk forskning,Medicinska fakulteten,Translational Neurology (TNY),Lund University Research Groups,WCMM-Wallenberg Centre for Molecular Medicine,Faculty of Medicine,Skåne University Hospital
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(creator_code:org_t)
- 2021-01-13
- 2021
- Engelska.
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Ingår i: Scientific Reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 11:1
- Relaterad länk:
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http://dx.doi.org/10... (free)
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https://www.nature.c...
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https://lup.lub.lu.s...
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https://doi.org/10.1...
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Abstract
Ämnesord
Stäng
- The pathological hallmark of Parkinson’s disease (PD) is the formation of Lewy bodies containing aggregated alpha-synuclein (α-syn). Although PD is associated with these distinct histological changes, other pathological features such as microvascular alterations have been linked to neurodegeneration. These changes need to be investigated as they create a hostile brain microenvironment and may contribute to the development and progression of the disease. We use a human α-syn overexpression mouse model that recapitulates some of the pathological features of PD in terms of progressive aggregation of human α-syn, impaired striatal dopamine fiber density, and an age-dependent motor deficit consistent with an impaired dopamine release. We demonstrate for the first time in this model a compromised blood–brain barrier integrity and dynamic changes in vessel morphology from angiogenesis at earlier stages to vascular regression at later stages. The vascular alterations are accompanied by a pathological activation of pericytes already at an early stage without changing overall pericyte density. Our data support and further extend the occurrence of vascular pathology as an important pathophysiological aspect in PD. The model used provides a powerful tool to investigate disease-modifying factors in PD in a temporal sequence that might guide the development of new treatments.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Medicinska och farmaceutiska grundvetenskaper -- Neurovetenskaper (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Basic Medicine -- Neurosciences (hsv//eng)
Publikations- och innehållstyp
- art (ämneskategori)
- ref (ämneskategori)
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