The risk of developing Alzheimer’s disease (AD) increases dramatically as we age. Similarly, the common malnutrition of zinc deficiency is also more prevalent in the elderly more due to changes in diet and zinc absorption as we age. We have shown that zinc deficiency induces the secretion of the inflammatory cytokine interleukin-1β (IL-1β) in macrophages and microglia. This is due to the activation of the IL-1β regulatory protein complex the NLRP3 inflammasome. Neuroinflammation has long been suspected as an exacerbating factor in AD pathology and recently the NLRP3 pattern recognition receptor (PRR) has been found to be the critical in regulated neuroinflammation in mouse models of AD. It is thought that AD associated toxic amyloid oligomers cause disruption in microglia physiology which initiates the formation of the multiprotein NLRP3 inflammasome complex causing the secretion of the IL-1 β. Therefore, this study aimed to assess whether a zinc deficient diet would accelerate the AD behavioural phenotype seen in the APPswe/PS1 mouse model of AD by inducing inflammation through NLRP3 activation. To test this hypothesis, mice were placed on a zinc deficient (3mg/kg) or a zinc normal (35mg/kg) diet for six months. Cognitive/memory performance was evaluated with the Morris water maze, Y-maze and novel smell tasks at baseline, three and six months on diet. To assess if the effect of zinc deficiency was reversible, at the 3 month time-point half the zinc deficient mice were placed back on a zinc normal diet. Our results suggest that zinc deficiency caused memory deficits in the APPswe/PS1 mice at 3 and 6 months on diet while at the same age the wild type mice on a zinc deficient diet and the APPswe/PS1 mice on normal diet showed no deficits. Furthermore, placing the zinc deficient mice on a zinc normal diet partially reverse the memory deficits. Additionally, it was found that innate immune cells from the zinc deficient mice had a hyper-inflammatory phenotype. Therefore, we have shown that zinc deficiency accelerates the AD phenotype in the APPswe/PS1 mice potentially through an inflammatory mechanism. This research aims to further investigate the role of zinc deficiency and NLRP3 in AD using NLRP3-/- mice and novel inhibitors of NLRP3 activation.