Targeting Neurovascular Unit Function May Improve Outcomes in Multiple Sclerosis

Therapeutics that modulate neurovascular unit function may benefit patients with multiple sclerosis, suggests a review article published online in Neurobiology of Disease.

“The neurovascular unit is a cellular network that controls neuroinflammation, maintains blood-brain barrier integrity, and tightly regulates cerebral blood flow, matching energy supply to neuronal demand,” wrote corresponding author Brad A Sutherland, PhD, of the University of Tasmania in Australia, and study coauthors. “The neurovascular unit is composed of vessel-associated cells such as endothelial cells, pericytes, and astrocytes, however neuronal and other glial cell types also comprise the neurovascular niche.”

In multiple sclerosis, cellular components in the neurovascular unit are negatively impacted, the authors reported. Single-cell transcriptomics data has identified compromised microvasculature cells in multiple sclerosis lesions, while large-scale genetic and small-scale cell biology studies imply neurovascular dysfunction could be a primary pathology with the development of multiple sclerosis.

The article reviewed current and emerging treatments that modulate neurovascular function, such as natalizumab, laquinimod, fingolimod, and glatiramer acetate, that may help patients with multiple sclerosis. More investigation is needed, however, to investigate whether targeting the neurovasculature could ease disease severity and protect against progression.

“Given that dysregulation of the neurovascular unit has the potential to impede effective remyelination and contribute to neurodegeneration, targeting the neurovascular unit should be considered in tandem with existing agents to improve outcomes of people with multiple sclerosis,” the authors advised.

Reference: 
Cashion JM, Young KM, Sutherland BA. How does neurovascular unit dysfunction contribute to multiple sclerosis? Neurobiol Dis. 2023;178:106028. doi:10.1016/j.nbd.2023.106028