The accumulation of amyloid-beta (Aβ) and phosphorylated tau (p-tau) proteins are known contributors to Alzheimer’s Disease (AD) pathogenesis, yet pharmacological interventions targeting these proteins have not been effective, indicating the involvement of additional molecular factors. These factors include lipid dyshomeostasis, altered energy and glucose metabolism, disturbed mitochondrial activity, oxidative stress, dysregulated cellular trafficking, and changes in neurotransmitter levels. Metabolomics, which reflects changes downstream of genomic, transcriptomic, and proteomic alterations, provides a sensitive measure of overall health by detecting endogenous metabolites, the final products of biochemical reactions.The Human Metabolome Database (HMDB) contains over 221,000 metabolites, including both water-soluble and lipid-soluble compounds. Metabolomics includes the study of polar metabolites (e.g., amino acids, carbohydrates) and lipids, with lipidomics focusing on the complete array of lipid classes. Metabolites serve as indicators of biochemical pathway changes in AD, and integrating genetic, transcriptomic, metabolomic, and proteomic data helps identify specific alterations. Two primary analytical techniques in metabolomics are mass spectrometry (MS) and nuclear magnetic resonance (NMR) spectroscopy. MS is favored for its sensitivity, selectivity, and ability to analyze a wide range of metabolites. Liquid chromatography-mass spectrometry (LC-MS) is particularly effective for diverse metabolites, offering comprehensive exploration of the metabolome. This chapter presents a summary of the results obtained from studies in this field.