Complement C3a Receptor (C3aR) Mediates Vascular Dysfunction, Hippocampal Pathology, and Cognitive Impairment in a Mouse Model of VCID.
Document Type
Article
Abstract
Vascular contributions to cognitive impairment and dementia (VCID) secondary to chronic mild-moderate cerebral ischemia underlie a significant percentage of cases of dementia. We previously reported that either genetic deficiency of the complement C3a receptor (C3aR) or its pharmacological inhibition protects against cerebral ischemia in rodents, while others have implicated C3aR in the pathogenesis seen in rodent transgenic models of Alzheimer's disease. In the present study, we evaluated the role of complement C3a-C3aR signaling in the onset and progression of VCID. We utilized the bilateral common carotid artery stenosis (BCAS) model to induce VCID in male C57BL/6 wild-type and C3aR-knockout (C3aR
Publication Date
3-8-2022
Publication Title
Transl Stroke Res
ISSN
1868-601X
PubMed ID
35258803
Digital Object Identifier (DOI)
10.1007/s12975-022-00993-x
Recommended Citation
Bhatia, Kanchan; Kindelin, Adam; Nadeem, Muhammad; Khan, Mohammad Badruzzaman; Yin, Junxiang; Fuentes, Alberto; Miller, Karis; Turner, Gregory H; Preul, Mark C; Ahmad, Abdullah S; Mufson, Elliott J; Waters, Michael F; Ahmad, Saif; and Ducruet, Andrew F, "Complement C3a Receptor (C3aR) Mediates Vascular Dysfunction, Hippocampal Pathology, and Cognitive Impairment in a Mouse Model of VCID." (2022). Translational Neuroscience. 1653.
https://scholar.barrowneuro.org/neurobiology/1653