Neurovascular dysfunction in the development and progression of neuroinflammatory diseases

Authors

• Jamila Gowdy, Robert H. Miller Laboratory, Department of Anatomy and Cell Biology, George Washington University, Washington, DC, United States.
• Julie Ahn, Robert H. Miller Laboratory, Department of Anatomy and Cell Biology, George Washington University, Washington, DC, United States.
• Robert H. Miller, Robert H. Miller Laboratory, Department of Anatomy and Cell Biology, George Washington University, Washington, DC, United States.
• Yusra Islam, Robert H. Miller Laboratory, Department of Anatomy and Cell Biology, George Washington University, Washington, DC, United States.

Document Type

Journal Article

Publication Date

1-1-2026

Journal

Frontiers in cellular neuroscience

Volume

20

DOI

10.3389/fncel.2026.1741928

Keywords

B cells; blood–brain barrier; endothelial dysfunction; glial cells; multiple sclerosis; neurodegeneration; neuroinflammation; neurovascular unit

Abstract

The neurovascular unit (NVU) is critical for brain homeostasis through its roles in maintenance of an effective blood brain barrier (BBB) and regulation of cerebral blood flow. Perturbation of the NVU is a hallmark of the pathology of multiple neurodegenerative diseases resulting in loss of BBB integrity, neuroinflammation and neuronal dysfunction. The NVU is a complex structure composed of endothelial cells, pericytes, as well as central nervous system (CNS) glial and neuronal components. While the importance of the CNS vasculature in health and disease is well established, the mechanisms underlying vascular pathology and its contributions to neurodegenerative diseases are less well defined. Neuroinflammation and reactive gliosis occurs in the majority of neurodegenerative diseases and recent studies suggest that immune mediated disruption of the BBB contributes to the induction of reactive gliosis and neuronal dysfunction. Potential consequences of NVU disruption include immune-driven vascular inflammation and leukocyte infiltration in Multiple Sclerosis (MS), protease-mediated tight junction degradation in ischemic stroke (IS), α-synuclein-associated endothelial dysfunction in Parkinson's Disease (PD), amyloid-β- and tau-induced pericyte injury in Alzheimer's Disease (AD), and complement-mediated vascular damage in Amyotrophic Lateral Sclerosis (ALS). Here we review the nature of NVU perturbations in these common neurodegenerative diseases, with an emphasis on the contribution of immune modulation of BBB disruption in neuropathology and disease progression.

APA Citation

Gowdy, Jamila; Ahn, Julie; Miller, Robert H.; and Islam, Yusra, "Neurovascular dysfunction in the development and progression of neuroinflammatory diseases" (2026). GW Authored Works. Paper 8880.
https://hsrc.himmelfarb.gwu.edu/gwhpubs/8880

Department

Anatomy and Regenerative Biology