Vascular Cognitive Impairment: Information from Animal Models on the Pathogenic Mechanisms of Cognitive Deficits

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F62690094%3A18470%2F19%3A50015656" target="_blank" >RIV/62690094:18470/19:50015656 - isvavai.cz</a>

Alternative codes found

RIV/00179906:_____/19:10394979 RIV/00159816:_____/19:00071074 RIV/00216208:11130/19:10394979 RIV/00216208:11150/19:10394979 RIV/00064203:_____/19:10394979

Result on the web

<a href="https://www.mdpi.com/1422-0067/20/10/2405/htm" target="_blank" >https://www.mdpi.com/1422-0067/20/10/2405/htm</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.3390/ijms20102405" target="_blank" >10.3390/ijms20102405</a>

Result language

angličtina

Original language name

Vascular Cognitive Impairment: Information from Animal Models on the Pathogenic Mechanisms of Cognitive Deficits

Original language description

Vascular cognitive impairment (VCI) is the second most common cause of cognitive deficit after Alzheimer&apos;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.

Czech name

—

Czech description

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Type

J_imp - Article in a specialist periodical, which is included in the Web of Science database

CEP classification

—

OECD FORD branch

30103 - Neurosciences (including psychophysiology)

Project

Result was created during the realization of more than one project. More information in the Projects tab.

Continuities

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Publication year

2019

Confidentiality

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Name of the periodical

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES

ISSN

1422-0067

e-ISSN

—

Volume of the periodical

20

Issue of the periodical within the volume

10

Country of publishing house

CH - SWITZERLAND

Number of pages

17

Pages from-to

1-17

UT code for WoS article

000471001400036

EID of the result in the Scopus database

2-s2.0-85066840764