Aim: Amyloid-beta (Aβ)-mediated neurotoxicity plays a pivotal role in the pathogenesis of Alzheimer's disease (AD), which induces oxidative stress and apoptosis. Linalool (LI) is a volatile monoterpene showing positive effect in AD treatment. This study was designed to research the protective effect of LI against neurotoxicity and cognitive deficits induced by Aβ1-40 in mice.
Main methods: Aβ1-40 (4μg) solution was injected in the bilateral hippocampus to induce cognitive deficits of mice. The protective effects of LI were evaluated by behavioral tests and the related mechanism was further explored by observing the apoptosis and oxidative stress changes in the hippocampus of mice.
Key findings: LI (100mg/kg, i.p.) administration significantly improved the cognitive performance of model mice in Morris water maze test and step-through test. Meanwhile, LI effectively reversed the Aβ1-40 induced hippocampal cell injury in histological examination, apoptosis in TUNEL assay, changes of oxidative stress indicators (SOD, GPX, AChE). Besides, the activated cleaved caspase (caspase-3, caspase-9) was suppressed and Nrf2, HO-1 expression was elevated by LI treatment.
Significance: LI could attenuate cognitive deficits induced by Aβ, and the neuroprotective effect of LI might be mediated by alleviation of apoptosis, oxidative stress depending on activation of Nrf2/HO-1 signaling. We could assume that LI has the potential to be a neuroprotective substance for AD therapy.
Keywords: Alzheimer's disease; Apoptosis; Cognitive improvement; Linalool; Oxidative stress.
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