Alzheimerâs disease is the most common form of senile dementia characterized pathologically by abnormally high levels of senile plaques composed of a 39-43 amino acid peptide known as Î²-Amyloid (AÎ²). The key event for the onset of Alzheimerâs is the aggregation of AÎ², resulting in a series of events which ultimately causes cell death. The mechanisms of toxicity of AÎ² are not fully understood, however it is thought to include membrane dysfunction/permeabalization, oxidative stress, mitochondria dysfunction etc. Within this study human neuroblastoma cells known as SH-SY5Y were used to study the effects of AÎ²42 in relation to metabolome of cells. Metabolomics is a field which combines strategies to attempt to identify and quantify all metabolites present intra-cellularly and extra-cellularly at a particular time and in a particular environment. Fourier transform infrared (FT-IR) spectroscopy was used in order to assess the phenotypic response of cells exposed to AÎ²42 peptide. This was used directly on cells (the metabolic fingerprint) and on the cell growth medium (the metabolic footprint). Gas chromatography - mass spectrometry and liquid chromatography â mass spectrometry were next used for metabolite profiling and identification. Multivariate and univariate analysis of data was carried out which showed phenotypic difference between control cells and cells exposed to AÎ²42. Results from FT-IR spectroscopy based analysis suggested specific metabolite changes within lipid, carbohydrate and nucleotide areas indicating that AÎ² could be causing damage to lipid structures as well as decreasing overall cell viability and numbers. Cells exposed to AÎ²42 also showed a more homogenous phenotype indicating that these cells could all have been arrested in one particular phase of the cell division cycle. Mass spectrometry results revealed poor separation of healthy and diseased samples based on multivariate analysis alone. Univariate analysis revealed up regulation of glutathione S-transferase P, adenosylmethionine decarboxylase and catechol O-methyltransferase by cells which could have been protective responses by the SH-SY5Y cells upon exposure to AÎ²42. Data suggested that a lipidomics approach would be useful and could possibly provide greater insight into metabolite changes in cells when exposed to AÎ²42.