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Astrocytes interact intimately with degenerating motor neurons in mouse amyotrophic lateral sclerosis (ALS).
Levine, J B; Kong, J; Nadler, M; Xu, Z.
Afiliación
  • Levine JB; Department of Psychiatry, University of Massachusetts Medical School, Worcester, MA 01655, USA.
Glia ; 28(3): 215-24, 1999 Dec.
Article en En | MEDLINE | ID: mdl-10559780
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.
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Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Astrocitos / Esclerosis Amiotrófica Lateral / Neuronas Motoras / Degeneración Nerviosa Límite: Animals / Humans Idioma: En Revista: Glia Asunto de la revista: NEUROLOGIA Año: 1999 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos
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Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Astrocitos / Esclerosis Amiotrófica Lateral / Neuronas Motoras / Degeneración Nerviosa Límite: Animals / Humans Idioma: En Revista: Glia Asunto de la revista: NEUROLOGIA Año: 1999 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos