Researchers have uncovered new evidence that lithium may play a protective role in preventing Alzheimer’s disease by mitigating the damaging effects of toxic amyloid plaques in the brain. A study conducted by Harvard Medical School and published in the journal Nature reveals that low lithium levels in the brain could be a significant contributing factor to the development of dementia. The research highlights that lithium, a naturally occurring substance in the body with various functions including mood regulation and neuroprotection, may be a ‘missing link’ in understanding Alzheimer’s risk.
The study, which tested lithium’s effects on both mice and human brain tissue, was conducted in collaboration with the Rush Memory and Aging Project in Chicago. This project provides post-mortem brain tissue from thousands of donors, allowing researchers to examine a wide range of cognitive health outcomes — from no dementia to advanced Alzheimer’s. The findings indicated that lithium levels decrease as signs of the disease progress, with the most significant reduction observed in patients with advanced Alzheimer’s.
According to the research, toxic amyloid plaques, a hallmark of Alzheimer’s, begin to interfere with lithium’s protective functions by attaching to it. When mice were placed on a lithium-restricted diet, their brains showed accelerated aging, increased amyloid-beta plaque formation, greater inflammation, memory loss, and cognitive decline. These findings suggest that maintaining natural lithium levels may be essential for preventing neurodegeneration and Alzheimer’s disease.
The researchers also discovered a new lithium compound — lithium orotate — which did not bind to amyloid, allowing it to restore memory and reverse brain damage, even in cases of advanced Alzheimer’s. Yankner, the senior author of the study, emphasized that lithium’s potential impact on multiple aspects of Alzheimer’s is significant, stating that ‘what impresses me the most is the widespread effect it has on the various manifestations of Alzheimer’s.’ He also noted that the idea that lithium deficiency could be a cause of Alzheimer’s is a novel concept, suggesting a new therapeutic approach. However, while the study indicates a possible link between lithium levels and amyloid beta buildup, it has limitations, including the use of animal models, which do not fully replicate the complexities of Alzheimer’s in humans.
Experts like Ozama Ismail, Ph.D., director of scientific programs for the Alzheimer’s Association, acknowledged the importance of these findings but emphasized that much more research is needed. ‘Studying mouse models is a vital early step in therapeutic research, but we need large clinical trials in representative populations to understand the health effects of lithium levels in the brain,’ Ismail said. He also predicted that future Alzheimer’s treatments will likely require a multifaceted approach, combining medication with lifestyle changes to improve outcomes. While the researchers agree that human clinical trials are necessary, they remain cautiously optimistic about the potential of lithium in combating this devastating disease.
As the scientific community continues to explore new potential treatments, the findings from this study could pave the way for future interventions, including the possibility of routine blood tests to screen for lithium levels and identify individuals at risk. However, Yankner warned against self-medication with lithium compounds, emphasizing that controlled clinical trials are essential to determine their safety and efficacy for Alzheimer’s patients. The study was supported by several organizations, including the National Institutes of Health and the Ludwig Family Foundation, underscoring the importance of collaborative research in advancing our understanding of neurological diseases.