Objectives To describe and critically evaluate the new research findings of Aron et al. on the relationship between lithium and Alzheimer’s dementia. To discuss the significance for future research and clinical practice. Methods Aron’s research group investigated lithium concentrations (derived from naturally ingested dietary lithium) in human brain tissue samples from deceased individuals with and without Alzheimer’s dementia, as well as in mouse models with and without Alzheimer’s pathology. In addition, the effects of a low-lithium diet and various lithium salts (in particular lithium carbonate and lithium orotate) on the development and progression of Alzheimer’s-typical changes were analysed. Results/Discussion Human samples showed a significantly reduced lithium concentration in the prefrontal cortex of Alzheimer’s patients, while an accumulation of lithium was detectable in the characteristic amyloid plaques. In mouse models, a low-lithium diet led to a deterioration in cognitive performance and development of Alzheimer’s pathology. It was particularly noteworthy that the administration of lithium orotate – in contrast to lithium carbonate – was able to prevent the formation and even induce regression of Alzheimer’s-typical changes in the mouse brain and memory tests. The effects were possibly mediated by changes in glycogen synthase kinase-3 beta (GSK3β), a key enzyme in Alzheimer’s pathogenesis. Conclusion The results point to a potential paradigm shift in Alzheimer’s research: naturally occurring lithium may have a physiological protective function for the ageing brain. Lithium orotate shows a pronounced neuroprotective and disease-modifying effect in preclinical models. Controlled clinical trials of lithium orotate in people with MCI or Alzheimer’s dementia are urgently needed to test the transferability of these spectacular findings.