Late onset hereditary cataract of the Emory mouse. A model for human senile cataract

The late onset cataract of the Emory mouse has appealed to many investigators as a useful animal model for human senile cataracts, and the finding that many earlier studies used a mixture of both early and late-onset forms should extend the usefulness of this animal model.

Abstract

The late onset cataract of the Emory mouse has appealed to many investigators as a useful animal model for human senile cataract. It has been the subject of about 15 publications, beginning in 1982. These have explored many features, including histology, chromatography and isoelectric focusing of the crystallins, enzyme profiles, amino acid and ion transport, membrane studies including changes in MP24 and MP26, analysis for a number of biochemical constituents, and its use as an assay system for testing the effect of anticataractogenic drugs and dietary restriction. These investigations have not uncovered a single metabolic lesion marked enough to be considered an important cause of this cataract. There is some evidence that the effect of oxidation may be a major factor; likewise there is evidence for faulty protein synthesis. In many cases, the changes in cataractogenesis appear to be accelerated aging changes. For this reason, any study of this cataract must employ age-matched controls of the cataract-resistant strain. A recent discovery is the finding that many earlier studies used a mixture of both early and late-onset forms, accounting for the wide variability in analytical results. The two substrains may have somewhat different applications in cataract research. Thus, the availability of these two substrains should extend the usefulness of this animal model.