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Relationship of microglial and astrocytic activation to disease onset and progression in a transgenic model of familial ALS
Glia, 1998-07, Vol.23 (3), p.249-256
Hall, Edward D.
Oostveen, Jo A.
Gurney, Mark E.
1998
Volltextzugriff (PDF)
Details
Autor(en) / Beteiligte
Hall, Edward D.
Oostveen, Jo A.
Gurney, Mark E.
Titel
Relationship of microglial and astrocytic activation to disease onset and progression in a transgenic model of familial ALS
Ist Teil von
Glia, 1998-07, Vol.23 (3), p.249-256
Ort / Verlag
New York: John Wiley & Sons, Inc
Erscheinungsjahr
1998
Quelle
Wiley Online Library - AutoHoldings Journals
Beschreibungen/Notizen
Transgenic mice that highly over‐express a mutated human CuZn superoxide dismutase (SOD1) gene [gly93→ala; TgN(SOD1‐G93A)G1H line] found in some patients with familial ALS (FALS) have been shown to develop motor neuron disease that is characterized by motor neuron loss in the lumbar and cervical spinal regions and a progressive loss of motor activity. The mutant Cu,Zn SOD exhibits essentially normal SOD activity but also generates toxic oxygen radicals as a result of an enhancement of a normally minor peroxidase reaction. Consequently, lipid and protein oxidative damage to the spinal motor neurons occurs and is associated with disease onset and progression. In the present study, we investigated the time course of microglial (major histocompatibility‐II antigen immunoreactivity) and astrocytic (glial fibrillary acidic protein immunoreactivity) activation in relation to the course of motor neuron disease in the TgN(SOD1‐G93A)G1H FALS mice. Four ages were investigated: 30 days (pre‐motor neuron pathology and clinical disease); 60 days (after initiation of pathology, but pre‐disease); 100 days (approximately 50% loss of motor neurons and function); and 120 days (near complete hindlimb paralysis). Compared to non‐transgenic littermates, the TgN(SOD1‐G93A)G1H mice showed significantly increased numbers of activated astrocytes (P < 0.01) at 100 days of age in both the cervical and lumbar spinal cord regions. However, at 120 days of age, the activation lost statistical significance. In contrast, microglial activation was significantly increased several‐fold at both 100 and 120 days. We hypothesize that astrocytic activation may exert a trophic influence on the motor neurons that is insufficiently maintained late in the course of the disease. On the other hand, the sustained, intense microglial activation may conceivably contribute to the oxidative stress and damage involved in the disease process. If true, then agents which inhibit microglia may help to limit disease progression. GLIA 23:249–256, 1998. © 1998 Wiley‐Liss, Inc.
Sprache
Englisch
Identifikatoren
ISSN: 0894-1491
eISSN: 1098-1136
DOI: 10.1002/(SICI)1098-1136(199807)23:3<249::AID-GLIA7>3.0.CO;2-#
Titel-ID: cdi_proquest_miscellaneous_16428276
Format
–
Schlagworte
Age Factors
,
ALS
,
Amyotrophic Lateral Sclerosis - genetics
,
Amyotrophic Lateral Sclerosis - pathology
,
Animals
,
astrocytes
,
Astrocytes - physiology
,
Biological and medical sciences
,
Biomarkers
,
Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases
,
Disease Progression
,
Glial Fibrillary Acidic Protein - analysis
,
Histocompatibility Antigens Class II - analysis
,
Humans
,
immunocytochemistry
,
Medical sciences
,
Mice
,
Mice, Transgenic
,
microglia
,
Microglia - physiology
,
Motor Neurons - pathology
,
Neurology
,
Nitric Oxide - metabolism
,
Oxidative Stress
,
Reactive Oxygen Species - metabolism
,
Recombinant Fusion Proteins - biosynthesis
,
spinal cord
,
Spinal Cord - pathology
,
Superoxide Dismutase - biosynthesis
,
Superoxide Dismutase - genetics
,
Superoxide Dismutase-1
,
Time Factors
,
transgenic mice
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