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    Astrocytes interact intimately with degenerating motor neurons in mouse amyotrophic lateral sclerosis (ALS)

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    Authors
    Levine, John B.
    Kong, Jiming
    Nadler, Mark
    Xu, Zuoshang
    UMass Chan Affiliations
    Neuroscience Program
    Department of Cell Biology
    Department of Pharmacology and Molecular Toxicology
    Department of Psychiatry
    Document Type
    Journal Article
    Publication Date
    1999-11-11
    Keywords
    Amyotrophic Lateral Sclerosis
    Animals
    Astrocytes
    Gliosis
    Humans
    Image Processing, Computer-Assisted
    Mice
    Mice, Transgenic
    Mitochondria
    Motor Neurons
    Mutation
    *Nerve Degeneration
    Reference Values
    Superoxide Dismutase
    Vacuoles
    Cell Biology
    Nervous System Diseases
    Neurology
    Neuroscience and Neurobiology
    Psychiatry
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    Link to Full Text
    http://dx.doi.org/10.1002/(SICI)1098-1136(199912)28:3<215::AID-GLIA5>3.0.CO;2-C
    Abstract
    Astrocytic proliferation and hypertrophy (astrogliosis) are associated with neuronal injury. However, neither the temporal nor the spatial relationship between astrocytes and injured neurons is clear, especially in neurodegenerative diseases. We investigated these questions in a mouse amyotrophic lateral sclerosis (ALS) model. The initial increase in astrogliosis coincided with the onset of clinical disease and massive mitochondrial vacuolation in motor neurons. After disease onset, astrogliosis increased further in parallel with the number of degenerating motor neurons. Examination of individual astrocytes by three-dimensional reconstruction revealed that astrocytes extended their processes toward, wrapped around, and sometimes penetrated vacuoles derived from neuronal mitochondria. These results show a close temporal correlation between the onset of neuronal degeneration and the beginning of astrogliosis in this neurodegenerative disease and reveal a novel spatial relationship that is consistent with the view that astrocytes play an active role in the neuronal degeneration process.
    Source
    Glia. 1999 Dec;28(3):215-24. DOI: 10.1002/(SICI)1098-1136(199912)28:3<215::AID-GLIA5>3.0.CO;2-C Link to article on publisher's site
    DOI
    10.1002/(SICI)1098-1136(199912)28:3<215::AID-GLIA5>3.0.CO;2-C
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/49229
    PubMed ID
    10559780
    Notes

    Medical student John B. Levine participated in this study as part of the Senior Scholars research program at the University of Massachusetts Medical School.

    Related Resources
    Link to Article in PubMed
    ae974a485f413a2113503eed53cd6c53
    10.1002/(SICI)1098-1136(199912)28:3<215::AID-GLIA5>3.0.CO;2-C
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