London, UK – August 15, 2025

In a potentially transformative breakthrough for neuroscience, a new study has established a direct link between low brain lithium levels and the onset of Alzheimer’s disease. The research, conducted by a team from Harvard Medical School and published in the journal Nature, shows for the first time that lithium is not merely a treatment for psychiatric disorders but plays an essential role in normal brain function. The groundbreaking discovery reveals that lithium is sequestered by toxic amyloid plaques, a key hallmark of Alzheimer’s, which depletes the mineral from brain tissue and may accelerate the disease’s progression. This unexpected finding offers a new direction for understanding how Alzheimer’s begins and could lead to innovative strategies for both early screening and prevention, providing fresh hope to millions affected by the devastating neurodegenerative condition.

The study, which examined brain tissue samples from deceased individuals with varying degrees of cognitive function, found that of all the trace metals analyzed, lithium was the only one that showed significantly different levels across the groups. Levels were high in cognitively healthy individuals but were greatly diminished in those with mild cognitive impairment and full-blown Alzheimer’s. This depletion was found to be one of the earliest changes leading to the disease. The researchers further demonstrated in mouse models that a lithium-deficient diet accelerated the aging process, giving rise to brain inflammation, loss of synaptic connections between neurons, and cognitive decline—all classic hallmarks of Alzheimer’s. The study’s implications are profound, suggesting that monitoring brain lithium levels could one day become a tool for early detection.

Key Headlines

 * Lithium Depletion Discovered: A new study establishes a direct link between low levels of lithium in the brain and the early onset of Alzheimer’s disease.

 * Amyloid Plaques Sequester Lithium: Researchers found that toxic amyloid-beta plaques, a hallmark of Alzheimer’s, bind to lithium, effectively trapping the mineral and depleting it from other brain cells.

 * New Research Direction: The findings suggest a novel pathway for the development of Alzheimer’s, opening the door to new preventive and therapeutic strategies.

 * Mouse Models Show Acceleration: In mouse models, a lithium-deficient diet was found to accelerate brain pathology and memory loss, confirming its role in driving the disease.

 * Potential for Early Screening: The study suggests that measuring brain lithium levels could eventually be used as an early screening tool for Alzheimer’s.

 * New Drug Compounds: Scientists identified a class of lithium compounds that can avoid capture by amyloid plaques and successfully restored memory in mice.

The Science Behind the Discovery and Its Impact

The researchers’ key finding is that the loss of lithium is not merely a consequence of Alzheimer’s but may be a causal factor. The team discovered that as amyloid-beta begins to form deposits in the early stages of dementia, it binds to lithium, significantly reducing its bioavailability in the brain. This lack of lithium impairs the function of crucial brain cell types, including microglia, the brain’s resident immune cells. Without sufficient lithium, microglia lose their ability to effectively degrade amyloid plaques, leading to a vicious cycle of increased plaque buildup and further lithium depletion. This process accelerates brain pathology and cognitive decline, all of which were successfully replicated in the mouse models.

While lithium has been used for decades as a mood stabilizer for bipolar disorder, its potential neuroprotective properties have been a subject of growing interest. Previous clinical trials using standard high doses of lithium carbonate for Alzheimer’s have shown mixed results and a high risk of side effects in elderly patients. This new research, however, points to a more promising avenue: maintaining physiological levels of lithium to prevent the disease from taking hold in the first place. The researchers were able to restore memory in mice by using a novel lithium compound that is designed to evade capture by amyloid plaques, providing a template for a new class of drugs that could be both effective and safe.

A New Horizon for Alzheimer’s Treatment

The findings provide a clear and compelling direction for future research. If confirmed in human clinical trials, the study suggests that a simple blood or cerebrospinal fluid test to measure lithium levels could be a vital new tool in the fight against Alzheimer’s. By identifying individuals at risk early, doctors could intervene with preventive measures, such as dietary changes or low-dose lithium supplements, before significant brain damage occurs. The prospect of a preventative strategy, rather than a treatment for an already advanced disease, is a major paradigm shift for the field.

The study has generated immense excitement within the scientific community, but experts caution that this is still an early stage of research.  While the link between lithium and Alzheimer’s is now stronger than ever, further research is needed to determine the ideal dosage and delivery method for lithium-based therapies in humans, especially given the potential toxicity of high doses. However, this breakthrough study represents a significant step forward, offering new hope that a simple element, long recognized for its therapeutic effects, may hold the key to unlocking the secrets of one of the most challenging diseases of our time.