Astrocytes interact intimately with degenerating motor neurons in mouse amyotrophic lateral sclerosis (ALS)
UMass Chan Affiliations
Neuroscience ProgramDepartment of Cell Biology
Department of Pharmacology and Molecular Toxicology
Department of Psychiatry
Document Type
Journal ArticlePublication Date
1999-11-11Keywords
Amyotrophic Lateral SclerosisAnimals
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
Metadata
Show full item recordAbstract
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 siteDOI
10.1002/(SICI)1098-1136(199912)28:3<215::AID-GLIA5>3.0.CO;2-CPermanent Link to this Item
http://hdl.handle.net/20.500.14038/49229PubMed ID
10559780Notes
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 PubMedae974a485f413a2113503eed53cd6c53
10.1002/(SICI)1098-1136(199912)28:3<215::AID-GLIA5>3.0.CO;2-C