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Neurotherapeutics. 2016 Oct;13(4):685-701. doi: 10.1007/s13311-016-0477-8.

Astrocytes: Integrative Regulators of Neuroinflammation in Stroke and Other Neurological Diseases.

Author information

1
Department of Neurology and Neurological Sciences, Stanford Medical School, Stanford, CA, 94305, USA.
2
Department of Neurology and Neurological Sciences, Stanford Medical School, Stanford, CA, 94305, USA. marion.buckwalter@stanford.edu.
3
Department of Neurosurgery, Stanford Medical School, Stanford, CA, 94305, USA. marion.buckwalter@stanford.edu.
4
Stanford Stroke Center, Stanford Medical School, Stanford, CA, 94305, USA. marion.buckwalter@stanford.edu.

Abstract

Astrocytes regulate neuroinflammatory responses after stroke and in other neurological diseases. Although not all astrocytic responses reduce inflammation, their predominant function is to protect the brain by driving the system back to homeostasis after injury. They receive multidimensional signals within the central nervous system and between the brain and the systemic circulation. Processing this information allows astrocytes to regulate synapse formation and maintenance, cerebral blood flow, and blood-brain barrier integrity. Similarly, in response to stroke and other central nervous system disorders, astrocytes detect and integrate signals of neuronal damage and inflammation to regulate the neuroinflammatory response. Two direct regulatory mechanisms in the astrocyte arsenal are the ability to form both physical and molecular barriers that seal the injury site and localize the neuroinflammatory response. Astrocytes also indirectly regulate the inflammatory response by affecting neuronal health during the acute injury and axonal regrowth. This ability to regulate the location and degree of neuroinflammation after injury, combined with the long time course of neuroinflammation, makes astrocytic signaling pathways promising targets for therapies.

KEYWORDS:

Astrocyte; Brain injury; Glial scar; Neuroinflammation; Stroke

PMID:
27677607
PMCID:
PMC5081110
DOI:
10.1007/s13311-016-0477-8
[Indexed for MEDLINE]
Free PMC Article

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