Behavioral and neurochemical alterations induced by vanillin in a mouse model of Alzheimer's disease

Abstract

Background and Objective: Alzheimer's disease (AD) is a progressive neurodegenerative disease where symptoms appear after significant neuronal loss. Current treatments for AD do not significantly alter the disease process, where they temporarily improve symptoms. In vitro data has indicated that low doses of vanillin reduce beta-amyloid aggregation and may possess cytoprotective effects. This research aimed to investigate the effect of vanillin on the AlCl3mouse model of AD and thus its possible usefulness in managing AD. Methodology: Male albino mice were divided into 8 groups of 10. Each group received different treatments of AlCl3, AlCl3+vanillin (30, 60 or 120 mg kg-1 day-1), vanillin alone and control. These experiments lasted for 30 days after which animals were subjected to behavioral and neurochemical assessment. Analysis was carried out using one way analysis of variance (ANOVA) with Dunnett's post test. Results: Lower doses of vanillin led to improvements in behavioral and neurochemical deficits induced by AlCl3. Conversely, a high dose of vanillin caused an exaggeration in the behavioral and neurochemical deficits induced by AlCl3. Furthermore, highest dose vanillin treatment, on its own, inflicted behavioral and neurochemical deficits comparable to those caused by AlCl3. Conclusion: It is concluded that vanillin negatively impacted cholinergic neuronal survival. Any marked benefits with lower doses of vanillin were attributed to its ability to indirectly increase synaptic acetylcholine abundance through blocking its degradation.