Complement C3a Receptor (C3aR) Mediates Vascular Dysfunction, Hippocampal Pathology, and Cognitive Impairment in a Mouse Model of VCID.
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
Transl Stroke Res
Digital Object Identifier (DOI)
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.