Mice transgenic for Alzheimer disease beta-amyloid develop lens cataracts that are rescued by antioxidant treatment.
Alzheimer disease is characterized by cerebral Abeta deposition, which we have recently discovered occurs also in the lens as cataracts in Alzheimer disease patients. Here we report the presence of significantly increased cataracts in the lenses of an Abeta-transgenic mouse model for Alzheimer disease and their amelioration upon treatment with EUK-189, a synthetic SOD/catalase mimetic. These data support an oxidative etiology for AD-associated lens cataracts and their potential to be treated preventatively with antioxidants.
Melov
Simon
S
Buck Institute for Age Research, 8001 Redwood Boulevard, Novato, CA 94945, USA. smelov@buckinstitute.org
Wolf
Norman
N
Strozyk
Dorothea
D
Doctrow
Susan R
SR
Bush
Ashley I
AI
D000544:Alzheimer Disease / Q000378:metabolism*; D016229:Amyloid beta-Peptides / Q000737:chemistry*; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D002374:Catalase / Q000494:pharmacology*; D002386:Cataract / Q000188:drug therapy* / Q000378:metabolism*; D005609:Free Radicals; D006801:Humans; D051379:Mice; D008822:Mice, Transgenic; D008956:Models, Chemical; D009942:Organometallic Compounds / Q000494:pharmacology*; D010100:Oxygen / Q000737:chemistry; D012459:Salicylates / Q000494:pharmacology*; D013482:Superoxide Dismutase / Q000378:metabolism
D016229:Amyloid beta-Peptides; D000975:Antioxidants; C436526:EUK-189; D005609:Free Radicals; D009942:Organometallic Compounds; D012459:Salicylates; D002374:Catalase; D013482:Superoxide Dismutase; D010100:Oxygen