The Emerging Roles of Ferroptosis in Vascular Cognitive Impairment

Vascular cognitive impairment (VCI) is a clinical syndrome that encompasses all forms of cognitive deficits caused by cerebrovascular disease, from mild cognitive impairment to dementia. Vascular dementia, the second most common type of dementia after Alzheimer's disease (AD), accounts for appr...

Full description

Saved in:
Bibliographic Details
Published inFrontiers in neuroscience Vol. 13; p. 811
Main Authors Yan, Nao, Zhang, Jun-Jian
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Research Foundation 06.08.2019
Frontiers Media S.A
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Vascular cognitive impairment (VCI) is a clinical syndrome that encompasses all forms of cognitive deficits caused by cerebrovascular disease, from mild cognitive impairment to dementia. Vascular dementia, the second most common type of dementia after Alzheimer's disease (AD), accounts for approximately 20% of dementia patients. Ferroptosis is a recently defined iron-dependent form of cell death, which is distinct from apoptosis, necrosis, autophagy, and other forms of cell death. Emerging evidence suggests that ferroptosis has significant implications in neurological diseases such as stroke, traumatic brain injury, and AD. Additionally, ferroptosis inhibition has an obvious neuroprotective effect and ameliorates cognitive impairment in various animal models. Here, we summarize the underlying mechanisms of ferroptosis and review the close relationship between ferroptosis and VCI.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
Edited by: Mohammad Badruzzaman Khan, Augusta University, United States
This article was submitted to Neurodegeneration, a section of the journal Frontiers in Neuroscience
Reviewed by: Akash George, University of Louisville, United States; Kenichi Shimada, Harvard Medical School, United States
ISSN:1662-4548
1662-453X
1662-453X
DOI:10.3389/fnins.2019.00811