An emerging role of astrocytes in vascular contributions to cognitive impairment and dementia

Brittani R. Price, Christopher M. Norris, Pradoldej Sompol, Donna M. Wilcock

Research output: Contribution to journalReview articlepeer-review

59 Scopus citations

Abstract

Vascular contributions to cognitive impairment and dementia (VCID) is understood to be the second most common cause of dementia after Alzheimer's disease, and is also a frequent comorbidity with Alzheimer's disease. While VCID is widely acknowledged as a key contributor to dementia, the mechanistic underpinnings of VCID remain poorly understood. In this review, we address the potential role of astrocytes in the pathophysiology of VCID. The vast majority of the blood vessels in the brain are surrounded by astrocytic end-feet. Given that astrocytes make up a significant proportion of the cells in the brain, and that astrocytes are usually passively connected to one another through gap junctions, we hypothesize that astrocytes are key mediators of cognitive impairment because of cerebrovascular disease. In this review, we discuss the existing body of literature regarding the role of astrocytes at the vasculature in the brain, and the known consequences of their dysfunction, as well as our hypotheses regarding the role astrocytes play in VCID. (Figure presented.). This article is part of the Special Issue “Vascular Dementia”.

Original languageEnglish
Pages (from-to)644-650
Number of pages7
JournalJournal of Neurochemistry
Volume144
Issue number5
DOIs
StatePublished - Mar 2018

Bibliographical note

Publisher Copyright:
© 2017 International Society for Neurochemistry

Keywords

  • Alzheimer's disease
  • astrocyte
  • dementia
  • glia
  • neurodegeneration
  • vascular dementia

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience

Fingerprint

Dive into the research topics of 'An emerging role of astrocytes in vascular contributions to cognitive impairment and dementia'. Together they form a unique fingerprint.

Cite this