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Review
. 2015 Apr 15;7(6):a020628.
doi: 10.1101/cshperspect.a020628.

Astrocytes in neurodegenerative disease

Affiliations
Review

Astrocytes in neurodegenerative disease

Hemali Phatnani et al. Cold Spring Harb Perspect Biol. .

Abstract

Astrocytes contribute to the maintenance of the health and function of the central nervous system (CNS). Thus, it is not surprising that these multifunctional cells have been implicated in the onset and progression of several neurodegenerative diseases. The involvement of astrocytes in the neuropathology of these diseases is likely a consequence of both the loss of normal homeostatic functions and gain of toxic functions. Intracellular aggregates in astrocytes are a common feature of various neurodegenerative diseases, and these aggregates perturb normal astrocytic functions in ways that can be harmful to neuronal viability. Here, we review the role of astrocytes in neurodegenerative diseases, focusing on their dysfunction in Huntington's disease (HD), Parkinson's disease (PD), Alzheimer's disease (AD), and amyotrophic lateral sclerosis (ALS).

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References

    1. Abramov AY, Canevari L, Duchen MR. 2003. Changes in intracellular calcium and glutathione in astrocytes as the primary mechanism of amyloid neurotoxicity. J Neurosci 23: 5088–5095. - PMC - PubMed
    1. Abramov AY, Canevari L, Duchen MR. 2004. β-Amyloid peptides induce mitochondrial dysfunction and oxidative stress in astrocytes and death of neurons through activation of NADPH oxidase. J Neurosci 24: 565–575. - PMC - PubMed
    1. Aebischer J, Cassina P, Otsmane B, Moumen A, Seilhean D, Meininger V, Barbeito L, Pettmann B, Raoul C. 2011. IFN-γ triggers a LIGHT-dependent selective death of motoneurons contributing to the non-cell-autonomous effects of mutant SOD1. Cell Death Differ 18: 754–768. - PMC - PubMed
    1. Allaman I, Gavillet M, Belanger M, Laroche T, Viertl D, Lashuel HA, Magistretti PJ. 2010. Amyloid-β aggregates cause alterations of astrocytic metabolic phenotype: Impact on neuronal viability. J Neurosci 30: 3326–3338. - PMC - PubMed
    1. Allaman I, Belanger M, Magistretti PJ. 2011. Astrocyte-neuron metabolic relationships: For better and for worse. Trends Neurosci 34: 76–87. - PubMed