Abstract
Alzheimer's disease (AD) pathogenesis is conditioned by the presence of amyloid beta (Aβ) and neuroinflammation. The gliovascular unit (GVU) illustrates the relationship between the vascular components of the brain and glial cells, particularly astrocytes, which are seen as critical elements mainly affected in this disease. In AD patients, the impairment of the GVU is seen as blood-brain barrier breakdown, decreased clearance of Aβ, and chronic inflammatory status. C-reactive protein (CRP) and its monomeric form (mCRP) are associated with endothelial dysfunction and amyloid plaque instability, contributing to neuroinflammation and neurodegeneration. The interconnections between the GVU and the dissociated form of CRP were demonstrated by mCRP implication in vascular permeability that supports inflammation and extravasation of pro-inflammatory cytokines into the brain parenchyma. Astrocytic activation and endfeet function alterations can exacerbate the progression of AD by elevating pro-inflammatory agents and vascular amyloid accumulations. This review aims to emphasize the synergistic link between the GVU and monomers of CRP in the perpetuation of the inflammatory status, exacerbating neurodegeneration and neuroinflammation. Understanding their implication in AD can bring insights into novel therapeutic strategies to reduce AD progression.