cumulation of Aβ42 peptide and attenuated paralysis.
The AIP-1 human homologue,AIRAPL, but not
AIRAP when expressed under the control of myo-
3 promoter also confers protection against Aβ toxicity
[18]. Both AIP-1 and AIRAPL contain a predicted
farnesylation site known to be critical for the
AIP-1-mediated longevity in C. elegans [19]. AIP-1
and AIRAPL enhance at least partially general protein
turnover by acting as positive regulators of
proteosomal function, and thus protect against Aβ-
induced toxicity [18].The effects of tetracycline and
its analogues doxycycline and minocycline on Aβ42-
induced toxicity were assayed [20] using the worms
expressing a temperature-inducible Aβ1–42 transgene
[21]. Tetracyclines successfully protected
transgenic worms from the Aβ insult by reducing
the concentration of oligomers considered to be responsible
for the toxic phenotype. These effects
were specific, dose-dependent and not linked to
any antibiotic activity. Furthermore, tetracyclines
protect Aβ-expressing nematodes from oxidative
stress by reducing the superoxide production, suggesting
a potential use of these drugs in targeting
Aβ aggregates.
cumulation of Aβ42 peptide and attenuated paralysis.The AIP-1 human homologue,AIRAPL, but notAIRAP when expressed under the control of myo-3 promoter also confers protection against Aβ toxicity[18]. Both AIP-1 and AIRAPL contain a predictedfarnesylation site known to be critical for theAIP-1-mediated longevity in C. elegans [19]. AIP-1and AIRAPL enhance at least partially general proteinturnover by acting as positive regulators ofproteosomal function, and thus protect against Aβ-induced toxicity [18].The effects of tetracycline andits analogues doxycycline and minocycline on Aβ42-induced toxicity were assayed [20] using the wormsexpressing a temperature-inducible Aβ1–42 transgene[21]. Tetracyclines successfully protectedtransgenic worms from the Aβ insult by reducingthe concentration of oligomers considered to be responsiblefor the toxic phenotype. These effectswere specific, dose-dependent and not linked toany antibiotic activity. Furthermore, tetracyclinesprotect Aβ-expressing nematodes from oxidativestress by reducing the superoxide production, suggestinga potential use of these drugs in targetingAβ aggregates.
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