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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
3
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pubmed:dateCreated |
2010-2-26
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pubmed:abstractText |
The main disease features of autosomal dominant optic atrophy (ADOA) are a bilateral reduction of visual acuity, cecocentral scotoma, and frequently tritanopia, which have been ascribed to a progressive loss of retinal ganglion cells (RGCs) and subsequent degeneration of the optic nerve. The main disease-causing gene is OPA1. Here, we examine a mouse carrying a pathogenic mutation in Opa1 by electrophysiological measurements and assess the fate of RGCs.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
1552-5783
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
51
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1424-31
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pubmed:meshHeading |
pubmed-meshheading:19834041-Animals,
pubmed-meshheading:19834041-Axonal Transport,
pubmed-meshheading:19834041-Cell Count,
pubmed-meshheading:19834041-Cell Survival,
pubmed-meshheading:19834041-Disease Models, Animal,
pubmed-meshheading:19834041-Electroretinography,
pubmed-meshheading:19834041-Evoked Potentials, Visual,
pubmed-meshheading:19834041-Fluorescent Dyes,
pubmed-meshheading:19834041-GTP Phosphohydrolases,
pubmed-meshheading:19834041-Mice,
pubmed-meshheading:19834041-Mice, Inbred C3H,
pubmed-meshheading:19834041-Mice, Inbred C57BL,
pubmed-meshheading:19834041-Microscopy, Fluorescence,
pubmed-meshheading:19834041-Optic Atrophy, Autosomal Dominant,
pubmed-meshheading:19834041-Optic Nerve,
pubmed-meshheading:19834041-Retina,
pubmed-meshheading:19834041-Retinal Ganglion Cells,
pubmed-meshheading:19834041-Stilbamidines,
pubmed-meshheading:19834041-Visual Acuity
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pubmed:year |
2010
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pubmed:articleTitle |
Electrophysiological and histologic assessment of retinal ganglion cell fate in a mouse model for OPA1-associated autosomal dominant optic atrophy.
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pubmed:affiliation |
Institute for Ophthalmic Research, Centre for Ophthalmology, University of Tübingen, Tübingen, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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