Purpose Cerebral hypo-metabolism,oxidative stress and β-amyloid peptide (Aβ) accumulation are key pathological events in Alzheimers disease (AD).β-secretase (BACE,i.e.,BACE 1),a prerequisite for Aβ genesis,is elevated in sporadic AD.Recent studies show BACE up-regulation in experimental conditions likely associated with energy insufficiency and/or oxidative stress.We investigated the effect of sublethal doses of mitochondrial respiratory inhibitors and potential endogenous oxidative substances on BACE expression in vivo using the retina as a model.Materials Retinas were analyzed biochemically and anatomically 48 h following intraocular applications of mitochondrial complex Ⅰ,Ⅱ and Ⅳ inhibitors including rotenone,3-nitropropionic acid and sodium azide,and plaque-containing oxidants including Fe3+ and Aβ42 fibrils (Aβ42f).