P27 Minimising the toxic effects of beta-Amyloid 42 on oxidative stress

Al Hussien-Ali, Pavlos Alifragis

Research output: Contribution to journalMeeting abstract


It is becoming increasingly apparent that the highly amyloidogenic beta-Amyloid 42 peptide is involved in various mechanisms which are instrumental to Alzheimer’s disease (AD) pathogenesis. Recent reports have shown that such a mechanism is the induction of oxidative stress early on in the disease process. It is believed that beta-Amyloid becomes a source of free radicals itself and this contributes to the initiation of lipid peroxidation, which modifies membrane fluidity and leads to disruption of mitochondrial metabolism, respiration and reactive oxygen species levels. Oxidative stress could be minimised using dietary or supplemented antioxidant therapies. Here we will discuss our findings regarding 12-oxo phytodienoic acid, jasmonic acid, and methyl jasmonate as antioxidant agents that can protect and E18 rat primary hippocampal neurons against beta-Amyloid 42 induced oxidative stress and toxicity. We report that all three compounds act as antioxidants and are able to reduce beta-Amyloid 42 induced increases in mitochondrial and nuclear ROS levels, however at varying potencies. The Jasmonates antioxidant capacities suggests that there is potential for use as an AD treatment however further research is currently underway to investigate other potential effects and to elucidate their specificity at reducing beta-Amyloid 42 induced toxicity.
Original languageEnglish
Pages (from-to)133-134
Number of pages2
JournalBiochemical Pharmacology
Early online date1 Aug 2017
Publication statusPublished - 1 Sept 2017

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