Macrophages come to mind as keys to cognitive decline
D.G. Harrison, Tomasz J. Guzik
D.G. Harrison, Tomasz J. Guzik
Published November 14, 2016
Citation Information: J Clin Invest. 2016;126(12):4393-4395. https://doi.org/10.1172/JCI91277.
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Commentary

Macrophages come to mind as keys to cognitive decline

Abstract

Cognitive impairment, an underappreciated consequence of hypertension, is linked to cerebral arteriolar disease through poorly defined mechanisms. A study by Faraco et al. in this issue of the JCI points to perturbations of neurovascular unit coupling caused by perivascular macrophages (PVMs) as a cause of hypertension-related cognitive impairment. Angiotensin II (Ang II) was shown to activate PVMs, causing them to produce superoxide and thereby alter the proper functioning of the adjacent arterioles. Faraco and colleagues also show that disruption of the blood-brain barrier occurs in hypertension, allowing circulating Ang II to access PVMs. This study provides important new insight into the role of inflammatory cells in the genesis of vascular dementia.

Authors

D.G. Harrison, Tomasz J. Guzik

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Figure 1

Proposed role of PVMs in cognitive dysfunction.

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Proposed role of PVMs in cognitive dysfunction. Hypertension leads to di...
Hypertension leads to disruption of the blood-brain barrier, allowing Ang II and probably other neurohumoral agents to stimulate the production of ROS, including superoxide (O2.–), by PVMs. Superoxide and other ROS promote vasoconstriction, endothelial dysfunction, and oxidative injury in cerebral arterioles. These events cause dysfunction of the NVU, leading to cognitive impairment. AT1R, AT1 receptor; BBB, blood-brain barrier.