October 5, 2025

Our brains contain lithium – and its loss could help drive Alzheimer’s disease, according to a study

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Alzheimer’s disease is one of the most cruel conditions that a person can develop. And even with recent advances, there is little to do once its symptoms emerge. Research this week could highlight a critical and previously missed factor at the origin of the disease, which could even lead to new treatments.

Scientists from the Harvard Medical School led the study, published Wednesday in Nature. By studying human brain samples and mice, they have found evidence that our brain naturally contains element lithium and that its deficiency can help explain the damage caused by Alzheimer. The results are well supported and may have discovered an important aspect of the neurological disorder, said an external expert in Gizmodo.

Study researchers “have carried out detailed and well designed studies to study how associated lithium levels (Alzheimer’s disease) at diagnostic, protein, cellular and gene level,” said Timothy Chang, neurologist at the University of California, Los Angeles who was not involved in the study. Chang is also director of California Alzheimer’s Disease Center at the UCLA.

The brain of people with Alzheimer’s is different in many ways of others. In particular, they contain high levels of poorly folded amyloid beta and tau, two proteins which normally have important functions. But these are not the only changes observed in Alzheimer’s disease. And it was by studying these other changes that Harvard researchers discovered.

With the help of existing projects that collected post-mortem tissue samples, they compared the levels of around 30 metals in the brain of people who died along the variable stages of cognitive health. The only major difference they found was with lithium. People with cognitively healthy brains had relatively high levels of lithium, while those with Alzheimer have much lower levels. Above all, this loss of lithium was apparent even in people who experienced light memory problems before dying.

Researchers have also studied healthy mice and genetically modified mice that develop a version of Alzheimer’s disease. When they have exhausted lithium from these mice, it seemed to speed up the accumulation of beta and unhealthy amyloid tau in the brain, as well as a decline in memory. They also found evidence that this loss is caused by beta amyloid plates linking lithium of the brain and that this loss of lithium seems to affect all the main types of brain cells negatively.

Although there has been limited research suggesting a possible link between lithium and Alzheimer’s disease, the authors say that the first is the first to show that our brain naturally carries it. In addition, their results suggest that lithium is essential for good brain health and that its absence is the key to Alzheimer’s development.

“This is the first study to suggest that lithium deficiency could contribute to Alzheimer’s disease. The reason why this has not been proposed is that it was not believed that lithium is a natural substance in the biological brain, just a drug with pharmacological effects with high doses of Bruce Yankner, professor of genetics and neurology of the Harvard, the Blavatnik Institute Blavatnik de la Harvard Blavatnik, of the Harvard Blavatnik, Blavatnik Institute of the Harvard Metal School of the Harvard Blavatnik Institute, said Gizmodo.

The implications of this study, although sooner, could certainly be dramatic. Yankner and his team were also able to identify a lithium -based compound which was not so easily linked by the amyloid beta version. And when they gave mice (healthy and mice mice with Alzheimer’s) this compound, it seemed to prevent harmful cerebral changes and the normally inevitable memory loss with the neurodegenerative condition. Even the best treatments based on amyloids for Alzheimer’s disease today, on the other hand, only modestly delay its progression.

Other forms of lithium are used in medicine to treat certain mental health disorders, in particular depression. But these versions require high doses to operate as expected and are accompanied by many side effects. The compound of the team, however, required a much lower dose to be effective in mice, and no sign of toxicity has been observed.

“Other clinical studies in humans would be necessary to assess whether the right type and the right dose of lithium can prevent or slow down Alzheimer’s disease,” said Chang.

Yankner and his team are now advancing with the research necessary to show that their compound (or something similar) can be safely tested in human clinical trials. But even before, the discovery of the team could bear fruit in other ways. It may be possible to detect the risk of Alzheimer’s in the future by measuring people’s lithium levels, for example. And there are still a lot of mysteries to unravel lithium and its role in the health of the brain.

“As a neuroscientist, I am delighted to explore the physiology of lithium in the brain,” said Yankner. “I suspect that we have just scratched the surface of what will be a very interesting biology.”


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