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Cerebral vessels: an overview of anatomy, physiology, and role in the drainage of fluids and solutes

Cerebral vessels: an overview of anatomy, physiology, and role in the drainage of fluids and solutes
Cerebral vessels: an overview of anatomy, physiology, and role in the drainage of fluids and solutes
The cerebral vasculature is made up of highly specialized structures that assure constant brain perfusion necessary to meet the very high demand for oxygen and glucose by neurons and glial cells. A dense, redundant network of arteries is spread over the entire pial surface from which penetrating arteries dive into the cortex to reach the neurovascular units. Besides providing blood to the brain parenchyma, cerebral arteries are key in the drainage of interstitial fluid (ISF) and solutes such as amyloid-beta. This occurs along the basement membranes surrounding vascular smooth muscle cells, toward leptomeningeal arteries and deep cervical lymph nodes. The dense microvasculature is made up of fine capillaries. Capillary walls contain pericytes that have contractile properties and are lined by a highly specialized blood–brain barrier that regulates the entry of solutes and ions and maintains the integrity of the composition of ISF. They are also important for the production of ISF. Capillaries drain into venules that course centrifugally toward the cortex to reach cortical veins and empty into dural venous sinuses. The walls of the venous sinuses are also home to meningeal lymphatic vessels that support the drainage of cerebrospinal fluid, although such pathways are still poorly understood. Damage to macro- and microvasculature will compromise cerebral perfusion, hamper the highly synchronized movement of neurofluids, and affect the drainage of waste products leading to neuronal and glial degeneration. This review will present vascular anatomy, their role in fluid dynamics, and a summary of how their dysfunction can lead to neurodegeneration.
1664-2295
Agarwal, Nivedita
8dffa34e-17c9-4858-93f9-e3b93915ddda
Carare, Roxana Octavia
0478c197-b0c1-4206-acae-54e88c8f21fa
Agarwal, Nivedita
8dffa34e-17c9-4858-93f9-e3b93915ddda
Carare, Roxana Octavia
0478c197-b0c1-4206-acae-54e88c8f21fa

Agarwal, Nivedita and Carare, Roxana Octavia (2021) Cerebral vessels: an overview of anatomy, physiology, and role in the drainage of fluids and solutes. Frontiers in Neurology, 11. (doi:10.3389/FNEUR.2020.611485).

Record type: Article

Abstract

The cerebral vasculature is made up of highly specialized structures that assure constant brain perfusion necessary to meet the very high demand for oxygen and glucose by neurons and glial cells. A dense, redundant network of arteries is spread over the entire pial surface from which penetrating arteries dive into the cortex to reach the neurovascular units. Besides providing blood to the brain parenchyma, cerebral arteries are key in the drainage of interstitial fluid (ISF) and solutes such as amyloid-beta. This occurs along the basement membranes surrounding vascular smooth muscle cells, toward leptomeningeal arteries and deep cervical lymph nodes. The dense microvasculature is made up of fine capillaries. Capillary walls contain pericytes that have contractile properties and are lined by a highly specialized blood–brain barrier that regulates the entry of solutes and ions and maintains the integrity of the composition of ISF. They are also important for the production of ISF. Capillaries drain into venules that course centrifugally toward the cortex to reach cortical veins and empty into dural venous sinuses. The walls of the venous sinuses are also home to meningeal lymphatic vessels that support the drainage of cerebrospinal fluid, although such pathways are still poorly understood. Damage to macro- and microvasculature will compromise cerebral perfusion, hamper the highly synchronized movement of neurofluids, and affect the drainage of waste products leading to neuronal and glial degeneration. This review will present vascular anatomy, their role in fluid dynamics, and a summary of how their dysfunction can lead to neurodegeneration.

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Published date: 13 January 2021

Identifiers

Local EPrints ID: 510887
URI: http://eprints.soton.ac.uk/id/eprint/510887
ISSN: 1664-2295
PURE UUID: 7b888158-2390-4a06-a60c-10025db3fc00
ORCID for Nivedita Agarwal: ORCID iD orcid.org/0000-0002-1387-9566
ORCID for Roxana Octavia Carare: ORCID iD orcid.org/0000-0001-6458-3776

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Date deposited: 23 Apr 2026 16:57
Last modified: 24 Apr 2026 02:05

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Author: Nivedita Agarwal ORCID iD

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