Statins are classically used in the treatment and prevention of hypercholesterolaemia due to their ability to inhibit the biosynthesis of cholesterol by blocking HMG-CoA-reductase, which is the rate limiting enzyme in cholesterol biosynthesis. Meanwhile, some studies have suggested the possible use of statins as potential therapeutics in the treatment of Alzheimer’s disease. Different pathways apart from their inhibitory activity on HMG-CoA-reductase have been explored. It has been shown that statins influence the release of β-amyloid, which aggregates to senile plaques, a pathological hallmark of AD. Although the mechanism has still not been fully discerned, it has been attributed to decreased cholesterol levels as well as decreased isoprenoid biosynthesis, which directly influences APP processing. NO-releasing substances have also been advocated to be of potential use in antidementive therapy due to their anti-inflammatory effect and their ability to improve the blood circulation. Notion behind this work was to determine the potential inhibitory effect of statins on β-amyloid-aggregation, as another possible pathway of their mode of action. Another goal was to prepare nitrate-statin-hybrid molecules in order to assess the extent to which the combination of these two promising pharmacophores would lead to a synergistic effect. Furthermore, some selected compounds were tested for their cholesterol-lowering and vasodilatory potencies to determine the influence of the structural modification on the biological activity. A novel nitratoacylated-stimvastatin derivative was obtained by cleaving the ester-side-chain, followed by selective protection of the lactonic alcohol and introduction of the nitrated-side-chain by acylation. Introduction of an organic nitrate to the simvastatin-scaffold resulted in only a slight decrease in the HMG-CoA-reductase inhibitory potency. In contrast, modification of the lactonic OH-group, which is crucial for inhibitory activity, either through acylation or elimination resulted in almost a complete loss of inhibitory potency. As expected all tested nitratoacylated compounds showed a vasodilatory effect. Since all tested derivatives encompass the same carrier molecule, the relaxation potency of the organic nitrates correlated with the number of nitrate groups in the molecule. In conclusion, the introduction of the bulky organic statin-scaffold did not result in a decrease of the vasodilatory potencies. A cell-free Aβ40-aggregation assay was successfully established, to investigate the possible direct effect of statin derivatives on β-amyloid-aggregation. For this purpose, the inhibitory activity of statins on Aβ40-aggregation was assessed as a function of the fluorescence of thioflavin T. The inhibitory activity, which was observed by the decrease of the measured fluorescence intensities, was further confirmed by electron microscopy.