Background: Alzheimer’s disease is the most common cause of dementia and remains a condition in which currently available treatments exert only limited influence on the underlying neurodegenerative process. Consequently, increasing attention has been directed toward factors that may modify disease progression, including lithium, a trace element with well-documented neurobiological properties. Objective: The aim of this review was to evaluate available preclinical evidence on the effects of lithium in the pathogenesis of Alzheimer’s disease, with particular emphasis on cognitive impairment and molecular mechanisms related to amyloid-β and tau pathology. Materials and methods: Original experimental studies human tissue, animal models, and in vitro systems were analysed. The review focused on investigations assessing the effects of low and subtherapeutic lithium doses on amyloid-β metabolism, tau phosphorylation, and cognitive performance. Results: Available data indicate a selective reduction of lithium levels in brain regions affected by Alzheimer-related pathology, accompanied by its sequestration within amyloid-β deposits. In animal models, lithium deficiency was associated with exacerbation of amyloid and tau pathology as well as deterioration of cognitive function. Restoration of physiological lithium levels, particularly through formulations with favourable bioavailability, was linked to attenuation of neurodegenerative changes. Conclusions: Lithium may play a significant role in the pathogenesis of Alzheimer’s disease, and disturbances in its homeostasis may contribute to the progression of neurodegeneration. Restoring physiological lithium levels represents a promising direction for further research on both preventive and therapeutic strategies for Alzheimer’s disease.