Original contributionMice transgenic for Alzheimer disease β-amyloid develop lens cataracts that are rescued by antioxidant treatment
Section snippets
Experimental procedures and results
Tg2576 (APP) mice were bred as previously described [1] and maintained under barrier conditions at the Buck Institute. Mice were treated with either vehicle (water) or the synthetic catalytic antioxidant EUK-189 [6] (30 mg/kg intraperitoneally, three times weekly) from 90 days of age through to 300–400 days of age, amounting to more than a year of continuous treatment in some mice. The structure and properties of EUK-189 have been described previously [6], [8], [9] (Fig. 1).
The age of the
Discussion
The observation of cataracts in Tg2576 mice, which recapitulates changes seen in patients with AD, encourages us to pursue the cataract phenotype in human subjects as a potential biomarker for AD [4]. Our findings also suggest that Aβ can induce sufficiently severe lens opacification, supporting the possibility that Aβ could participate in age-related cataracts, the most common form of blindness. Intriguingly, early onset cataracts and AD are common comorbid conditions in Down syndrome[13] and
Acknowledgments
This work was supported by grants from the NIA (RO1AG18679 to S.M., RO1AG12686 to A.I.B.), Alzheimer's Association (to A.I.B.), NHMRC (A.I.B.), and NEI (RO1EY11733 to N.W.) and an award from the Institute for the Study of Aging to S.M. and an Ellison Scholar Award to S.M. S.M. is indebted to N. Nagulko and other members of the Melov laboratory for excellent animal care. All animal procedures were carried out under approved institutional animal protocols at the Buck Institute. Ashley I. Bush is
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