Glial cell response after aneurysmal subarachnoid hemorrhage - Functional consequences and clinical implications

Publication date

2016-03-01

Authors

van Dijk, Bart
Vergouwen, Mervyn D IISNI 0000000393548675
Kelfkens, Myrna M.
Rinkel, Gabriel J EISNI 0000000388847590
Hol, EllyORCID 0000-0001-5604-2603

Editors

Advisors

Supervisors

Document Type

Article

Collections

Open Access logo

License

taverne

Abstract

Glial cells, both astrocytes andmicroglia, respond to neurodegenerative processes and to brain damage by a process called reactive gliosis. This response is highly context dependent, varies frommild to severe, and can be protective or detrimental for neural functioning. In patients with a subarachnoid hemorrhage from a ruptured aneurysm, the acute glial response is important to restrict the initial damage. Patients who survive the hemorrhage and early brain injury,oftensuffer fromdelayedcerebral ischemia or persisting cognitive impairment.Glia emerge as versatile cells that can modulate synapses and can control the microcirculatory blood flow in the brain. Therefore, a sustained activation of glial cells can affect normal brain functioning. Here we review the current literature on the glial response induced by aneurysmal subarachnoid hemorrhage in humans and in animal models. We discuss how reactive gliosis can affect brain functioning and how it may contribute to early brain injury, delayed cerebral ischemia and cognitive impairment after aneurysmal subarachnoid hemorrhage. This article is part of a Special Issue entitled: Neuro Inflammation edited by Helga E. de Vries and Markus Schwaninger.

Keywords

Astrocytes, Cognitive impairment, Microglia, Reactive gliosis, Stroke, Subarachnoid hemorrhage, Taverne, Molecular Biology, Molecular Medicine, Journal Article

Citation

van Dijk, B J, Vergouwen, M D I, Kelfkens, M M, Rinkel, G J E & Hol, E M 2016, 'Glial cell response after aneurysmal subarachnoid hemorrhage - Functional consequences and clinical implications', Biochimica et Biophysica Acta. Molecular Basis of Disease, vol. 1862, no. 3, pp. 492-505. https://doi.org/10.1016/j.bbadis.2015.10.013