"Alzheimer’s disease (AD) is a neurodegenerative disorder that advances through a unique cascade of characteristic neuropathological features. Distinguishing features include the accumulation of amyloid beta plaques and neurofibrillary tangles (NFTs) in the brain, accompanied by learning and memory impairments. The disease is projected to begin years-to-decades before clinical diagnosis. Accordingly, prodromal biomarkers are a necessity with early diagnosis as the goal. Neurochemical measures obtained via non-invasive brain imaging have potential to serve as early, AD biomarkers. Evidence suggests that alterations in the concentrations of certain metabolites are related to inflammation. It is known that while inflammation is ubiquitous in the progressed disease state, it is also apparent during initial stages. Of interest, a paradoxical increase in neuronal activity during early stages of AD has been noted, with a suspected link to an initial inflammatory response via proinflammatory cytokines. Early evidence suggests that alongside their role in immune mediation, cytokines play a critical part in maintaining optimal synaptic activity, and that early deviations from this role may contribute directly to downstream AD pathogenesis. Therefore, as magnetic resonance spectroscopy (MRS) has the capacity to noninvasively quantify neurochemical concentrations, it is an appropriate tool to pinpoint early fluctuations associated with inflammation and elevated cytokine activation.A greater understanding of AD requires an improved appreciation for its initial evolution. This requires, not only investigation into potential preclinical, neurochemical biomarkers, but furthermore, an examination into any parallel cognitive deficits. This project investigated prodromal AD in a transgenic (Tg) rodent model from early adulthood to middle age. It utilized in vivo proton magnetic resonance spectroscopy (1H MRS) to assess longitudinal changes in neurochemistry and the Barnes maze (BM) to evaluate spatial learning and memory. The central research objective was the longitudinal characterization of neurochemistry and behaviour in the TgF344-AD rodent model during the initial disease state, to highlight abnormalities that precede diagnosable AD.The study was conducted from approximately 4 to 10 months of age, in both TgF344-AD rats and their wildtype (WT) controls. Five evenly spaced magnetic resonance (MR) scans were acquired during this time (1 every 6 weeks), in addition to three sessions of behavioural testing (1 every 2 months). The BM was implemented to test spatial learning and memory ability, and longitudinal changes in metabolic levels were evaluated through linear mixed effects modeling.Altered neurochemistry was recorded between genotypes and across time in prodromal stages of AD. More specifically, Tg rats had significantly lower levels of glutamine (Gln), a precursor to glutamate (Glu), following disease initiation and increasing with age. In addition, with time Glu levels fell and myo-inositol (Ins) levels rose, independent of genotype. N-acetyl aspartate (NAA), reportedly reduced at later stages of AD, remained unchanged in Tg relative to WT rats. Neurochemical changes were not accompanied by a significant loss in cognitive ability, and thus appear to precede characteristic cognitive impairments.This research demonstrates that altered neurochemistry materializes in early AD and occurs before the onset of measurable behavioural deficits. A better understanding of preclinical AD requires further investigation into the relationship between neurochemistry, cognition, neuroanatomy, and the concentrations of proinflammatory mediators. Consequently, this could contribute to novel diagnostic and treatment techniques through the identification of reliable, early biomarkers"--