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1 elevant bioactive metal chelators related to clioquinol.
2 c metal chelating agents desferrioxamine and clioquinol.
3 howed decreased cell death when treated with clioquinol.
4 ch was inhibited by Cu2+ chelators including clioquinol.
5 brain rose by about 15% in mice treated with clioquinol.
6 n, cholesterol, and the proposed efficacy of clioquinol.
7 led trial in 36 patients with AD showed that clioquinol (250-750 mg daily) reduced plasma concentrati
8 xin rotenone and opposed by those induced by clioquinol, a compound with demonstrated therapeutic eff
9 tion (iAbeta5, a beta-sheet breaker peptide; clioquinol, a copper-zinc chelator) on the ability of is
12 ly, in a tissue culture model, we found that clioquinol, a metal chelator in clinical trials for AD t
14 ington's disease, we examined the effects of clioquinol, a metal-binding compound currently in clinic
17 view examines the recent studies relating to Clioquinol and AD, and anticipates the imminent results
18 Finally, the Abeta aggregation inhibitor clioquinol and gamma-secretase inhibitor L-685,458 atten
19 ell death, and contrary to previous reports, clioquinol and other hydroxyquinoline compounds do not a
20 4 and 3.2 microM, respectively) compared to clioquinol and pyrrolidine dithiocarbamate (IC50 of 10 a
22 We report here that after binding to copper, clioquinol can inhibit the proteasomal chymotrypsin-like
26 istration of the bioavailable metal chelator clioquinol (CQ) on susceptibility to the Parkinson's-ind
30 istration of the bioavailable iron chelator, clioquinol (CQ), to older mice was found to protect agai
32 ed 9 week study of a mouse model of AD, oral clioquinol decreased brain Abeta by 49% without systemic
34 s, such as desferrioxamine (Fe chelator) and clioquinol (Fe, Cu, and Zn chelator), which reduce Abeta
35 ises the issue of specific iron chelators or clioquinol for control of oxidative damage in Parkinson'
37 mplexes were also >100-fold more potent than clioquinol in a tumor spheroid model, with values simila
41 ver, dihydrotestosterone partially inhibited clioquinol-induced AR suppression and apoptosis only in
43 ain deposits in vitro and one such compound, clioquinol, inhibits Abeta deposition in the Tg2576 mous
50 dition of dihydrotestosterone did not affect clioquinol-mediated proteasome inhibition in both prosta
54 by ferritin transgene or the metal chelator clioquinol prevent oxidative damage and MPTP toxicity in
56 he reduced heme site, and (3) chelators like clioquinol remove Cu from these aggregates, while drugs
59 he Abeta aggregation inhibitors, iAbeta5 and clioquinol, selectively attenuated caspase-3 activation
60 perturbing amyloid's metallo-chemistry, and Clioquinol treatment has been shown to be beneficial in
65 Moreover, the Abeta aggregation inhibitor, clioquinol, was able to attenuate isoflurane-induced cas
66 ease was inhibited by in vivo treatment with clioquinol, which suggests that brain Abeta accumulation
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