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Vascular Cognitive Impairment: Information from Animal Models on the Pathogenic Mechanisms of Cognitive Deficits
J. Hort, M. Vališ, K. Kuča, F. Angelucci,
Jazyk angličtina Země Švýcarsko
Typ dokumentu časopisecké články, přehledy
NLK
Directory of Open Access Journals
od 2000
Free Medical Journals
od 2000
Freely Accessible Science Journals
od 2000
PubMed Central
od 2007
Europe PubMed Central
od 2007
ProQuest Central
od 2000-03-01
Open Access Digital Library
od 2000-01-01
Open Access Digital Library
od 2007-01-01
Health & Medicine (ProQuest)
od 2000-03-01
ROAD: Directory of Open Access Scholarly Resources
od 2000
PubMed
31096580
DOI
10.3390/ijms20102405
Knihovny.cz E-zdroje
- MeSH
- Alzheimerova nemoc metabolismus MeSH
- amyloidní beta-protein metabolismus MeSH
- astrocyty metabolismus MeSH
- cytokiny metabolismus MeSH
- endoteliální buňky metabolismus MeSH
- insulinu podobný růstový faktor I metabolismus MeSH
- kognice * MeSH
- kognitivní dysfunkce metabolismus patologie MeSH
- lidé MeSH
- mikroglie metabolismus MeSH
- modely u zvířat MeSH
- mozek metabolismus MeSH
- oxid dusnatý MeSH
- oxidační stres MeSH
- pericyty metabolismus MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
Vascular cognitive impairment (VCI) is the second most common cause of cognitive deficit after Alzheimer's disease. Since VCI patients represent an important target population for prevention, an ongoing effort has been made to elucidate the pathogenesis of this disorder. In this review, we summarize the information from animal models on the molecular changes that occur in the brain during a cerebral vascular insult and ultimately lead to cognitive deficits in VCI. Animal models cannot effectively represent the complex clinical picture of VCI in humans. Nonetheless, they allow some understanding of the important molecular mechanisms leading to cognitive deficits. VCI may be caused by various mechanisms and metabolic pathways. The pathological mechanisms, in terms of cognitive deficits, may span from oxidative stress to vascular clearance of toxic waste products (such as amyloid beta) and from neuroinflammation to impaired function of microglia, astrocytes, pericytes, and endothelial cells. Impaired production of elements of the immune response, such as cytokines, and vascular factors, such as insulin-like growth factor 1 (IGF-1), may also affect cognitive functions. No single event could be seen as being the unique cause of cognitive deficits in VCI. These events are interconnected, and may produce cascade effects resulting in cognitive impairment.
Citace poskytuje Crossref.org
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- $a Hort, Jakub $u Memory Clinic, Department of Neurology, 2nd Faculty of Medicine, Charles University and Motol University Hospital, 150 06 Prague, Czech Republic. jakub.hort@gmail.com. International Clinical Research Centre, St. Anne's University Hospital, 656 91 Brno, Czech Republic. jakub.hort@gmail.com.
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- $a Vascular cognitive impairment (VCI) is the second most common cause of cognitive deficit after Alzheimer's disease. Since VCI patients represent an important target population for prevention, an ongoing effort has been made to elucidate the pathogenesis of this disorder. In this review, we summarize the information from animal models on the molecular changes that occur in the brain during a cerebral vascular insult and ultimately lead to cognitive deficits in VCI. Animal models cannot effectively represent the complex clinical picture of VCI in humans. Nonetheless, they allow some understanding of the important molecular mechanisms leading to cognitive deficits. VCI may be caused by various mechanisms and metabolic pathways. The pathological mechanisms, in terms of cognitive deficits, may span from oxidative stress to vascular clearance of toxic waste products (such as amyloid beta) and from neuroinflammation to impaired function of microglia, astrocytes, pericytes, and endothelial cells. Impaired production of elements of the immune response, such as cytokines, and vascular factors, such as insulin-like growth factor 1 (IGF-1), may also affect cognitive functions. No single event could be seen as being the unique cause of cognitive deficits in VCI. These events are interconnected, and may produce cascade effects resulting in cognitive impairment.
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