Molecular Neurobiology

, Volume 38, Issue 3, pp 231–241

Targeted Activation of Astrocytes: A Potential Neuroprotective Strategy

Article

DOI: 10.1007/s12035-008-8043-y

Cite this article as:
Escartin, C. & Bonvento, G. Mol Neurobiol (2008) 38: 231. doi:10.1007/s12035-008-8043-y

Abstract

Astrocytes are involved in many key physiological processes in the brain, including glutamatergic transmission, energy metabolism, and blood flow control. They become reactive in response to pathological situations, a response that involves well-described morphological alterations and less characterized functional changes. The functional consequences of astrocyte reactivity seem to depend on the molecular pathway involved and may result in the enhancement of several neuroprotective and neurotrophic functions. We propose that a selective and controlled activation of astrocytes may switch these highly pleiotropic cells into therapeutic agents to promote neuron survival and recovery. This may represent a potent therapeutic strategy for many brain diseases in which neurons would benefit from an increased support from activated astrocytes.

Keywords

Reactive astrocytesActivation of astrocytesBrain diseasesTherapeutic targetCytokines

Abbreviations

AD

Alzheimer’s disease

ALS

Amyotrophic lateral sclerosis

BrdU

Bromodeoxyuridine

CNTF

Ciliary neurotrophic factor

COX2

Cyclooxygenase 2

GFAP

Glial fibrillary acidic protein

FGF

Fibroblast growth factor

KO

Knockout

HD

Huntington’s disease

IGF-1

Insulin-like growth factor 1

IL

Interleukin

iNOS

Inducible nitric oxide synthase

LPS

Lipopolysaccharide

MCAO

Middle cerebral artery occlusion

MRI

Magnetic resonance imaging

NGF

Nerve growth factor

NFκB

Nuclear factor-κ B

NMDA

N-Methyl-d-aspartate

PET

Positron emission tomography

STAT3

Signal transducer and activator of transcription 3

SOCS3

Suppressor of cytokine signaling 3

SOD

Superoxide dismutase

SCI

Spinal cord injury

TGFβ

Transforming growth factor β

TNFα

Tumor necrosis factor α

Copyright information

© Humana Press Inc. 2008

Authors and Affiliations

  1. 1.CEA, IB2M, MIRCen, CNRS URA2210OrsayFrance
  2. 2.Department of NeurologyUCSF and VA Medical CenterSan FranciscoUSA