Recent research suggests that a lithium deficiency in the brain may be the primary cause of Alzheimer's disease. A team from Harvard University discovered that beta-amyloid proteins reduce lithium concentration, weakening its neuroprotective effects; however, lithium orotate can prevent this phenomenon and reverse memory degradation in mouse experiments. These findings, published in Nature, may in the future enable early dementia screening through lithium concentration testing and the development of novel treatment strategies using lithium orotate.
Lithium deficiency in the brain may be the main cause of Alzheimer's disease.
Lithium, the lightest metal and also the lightest solid element, was once added to soda to uplift people's mood upon consumption, and has been formulated into medications for treating manic-depressive disorder and depression. However, its most well-known application is undoubtedly in lithium batteries. A recent study has discovered that this versatile metal has another potential function: treating Alzheimer's disease.
Alzheimer's disease, also known as dementia, is a slowly progressing neurodegenerative disease that worsens over time, affecting approximately 400 million people worldwide. With the global trend of aging population, this number will continue to rise, making it a healthcare issue that cannot be ignored.
The main symptom of Alzheimer's disease is memory loss, but what is the initial trigger?
Why do some people with similar brain changes gradually lose their memory while others do not? This question has puzzled neuroscientists for decades. Now, a group of scientists from Harvard University in the United States may have found the answer: a lack of lithium in the brain.
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Existing Alzheimer's disease treatments can only delay, not reverse, the condition.
This paper, published in the journal *Nature* on August 6, 2025, confirms for the first time that this naturally occurring metal in the brain can protect it from neurodegeneration and maintain the normal functioning of all major brain cells.
This significant research finding has reorganized our decades-long observations of Alzheimer's disease, providing a new theoretical foundation for the disease and offering brand-new strategies for early diagnosis, prevention, and treatment.
Perhaps in the near future, by routinely drawing blood to test the brain lithium levels, we can identify early on individuals who belong to the potentially high-risk group for Alzheimer's disease, enabling early prevention and treatment.
Recent studies have shown that Alzheimer's disease involves a series of brain abnormalities, such as the aggregation of beta-amyloid proteins, neurofibrillary tangles of tau proteins, and the deficiency of a protective protein named REST; however, these abnormalities do not fully explain the etiology of the disease.
For instance, some individuals detected with the aforementioned abnormalities do not exhibit signs of cognitive decline; moreover, treatments recently developed targeting beta-amyloid proteins generally cannot reverse memory loss but only slightly slow down the rate of cognitive decline. From these phenomena, it is not hard to see that genetics and environment can influence the risk of developing Alzheimer's disease, yet scientists still do not understand why some individuals with risk factors develop the disease while others do not.
Lithium orotate shows hope of reversing Alzheimer's disease in mice
Bruce Yankner, the corresponding author of this paper and a professor of genetics and neurology at the Blavatnik Institute at Harvard Medical School, said that lithium might be the crucial missing link.
He believes that a lack of sufficient lithium in the brain may be the cause of Alzheimer's disease, which is a very novel viewpoint and also outlines a completely different treatment approach. He said that this research has kindled our hope that perhaps one day scientists could comprehensively treat this disease with drugs containing lithium, rather than just focusing on single aspects such us the original text seems incomplete here
A research team from Harvard University discovered in human and mouse models that when beta-amyloid begins to form deposits in the early stages of Alzheimer's disease, it binds to lithium, reducing lithium concentration and thereby diminishing lithium's neuroprotective function in the brain, triggering symptoms such as memory loss.
They simultaneously discovered that lithium orotate, a lithium compound, does not bind to beta-amyloid protein. Using lithium orotate to treat mice can reverse the progression of Alzheimer's disease, prevent brain cell damage, and restore memory. Bruce Yankner stated that one of their most exciting findings was that even extremely low doses of lithium orotate could produce significant effects.