Alzheimer’s disease linked to lithium deficiency in a new Harvard study

Researchers have discovered a new factor that could contribute to the development of Alzheimer’s disease.

A study by the Harvard Medical School identified low levels of lithium in the brain as a possible trigger for common dementia.

Lithium is known to have many functions in the brain, especially in balance the chemicals regulating mood, protecting neurons and management of emotional treatment. It has also been used to treat bipolar disorders and depression.

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Now, new discoveries show that metal could be a “missing link” at the risk of Alzheimer’s, according to a press release from Harvard.

Researchers have tested the effects of lithium in mice, as well as human brain tissue and blood samples.

In a model of mouse of Alzheimer’s disease, a lithium deficiency, on the right, considerably increased the beta amyloid deposits in the brain compared to the mice which had normal physiological levels of lithium, on the left. Lower row: the same goes for the neurofibrillary tape of Alzheimer’s neurofibrillar. (Yankner Lab)

Human brain samples have been obtained in partnership with the Rush Memory and Agging project in Chicago, which maintains the post -mortem cerebral tissues of thousands of donors.

The samples represented the complete spectrum of cognitive health, ranging from any signs of illness to a slight cognitive impairment to advanced Alzheimer, according to the Liberation.

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They discovered that lithium levels became lower as signs of the disease increased, showing “considerably decreased” in advanced Alzheimer’s patients.

“This is the first time that anyone has shown that lithium has existed at a natural level which is biologically significant without giving it as a medication.”

While toxic amyloid plates accumulate in the brain – a characteristic of Alzheimer’s – they begin to attach to lithium, preventing him from performing his protection functions.

When the mice have been fed by a “limited lithium diet”, the lithium levels of their brains have decreased, causing accelerated aging, the formation of amyloid-bêta plates, greater inflammation, memory loss and cognitive decline.

A lithium deficiency cleared up the myelin which coat the neurons, on the right, compared to normal mice. (Yankner Lab)

“Lithium turns out to be like other nutrients that we obtain from the environment, such as iron and vitamin C,” said the main author Bruce Yankner, professor of genetics and neurology at the Blavatnik Institute of the Harvard Medical School, in the press release.

“This is the first time that anyone has shown that lithium has existed at a natural level which is biologically significant without giving it as a medication.”

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The researchers also discovered a new type of lithium compound – Lithium orotate – which was not linked to the amyloid. When mice drank water containing this compound, it helped restore memory and reverse brain damage, even for those who had advanced disease signs.

The results were published in the journal Nature.

The brain tissue samples represented the complete spectrum of cognitive health, ranging from any signs of illness to a slight cognitive impairment to the advanced Alzheimer’s disease. (istock)

“What impresses me most with lithium is the widespread effect he has on the various Alzheimer’s demonstrations,” said Yanker. “I really saw nothing like this during all my years of work on this disease.”

“The idea that lithium deficiency could be a cause of Alzheimer’s disease is new and suggests a different therapeutic approach.”

Potential limitations

Although the study suggested that the quantity of lithium in the brain could be linked to the accumulation of amyloid beta, it had obvious limits, according to Ozama Ismail, Ph.D., director of scientific programs for the Alzheimer association in Chicago.

Although studies on mouse models are an “essential step in therapeutic research, the author of the main study stressed that much more research is necessary to understand the health effects of lithium levels in the brain. (istock)

“Animal models do not directly reproduce Alzheimer’s disease in humans; they can rather provide information on the biology of progression and the development of the disease,” said Ismail, which was not involved in the study, at Fox News Digital.

“Mouse models have been modified to accumulate amyloid beta, a characteristic protein that accumulates in the brain of people with Alzheimer’s.”

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Although studies on mouse models are an “essential step in therapeutic research, Ismail has stressed that much more research is necessary to understand the effects on the health of lithium levels in the brain.

“Understand whether lithium can be therapeutic for Alzheimer’s disease requires major clinical trials in representative populations,” he said.

If future studies confirm these results, scientists say that routine blood tests could potentially detect lithium levels and identify people at risk. (istock)

Like other major diseases, it is likely that the treatment of Alzheimer’s will require several approaches combining changes in medication and lifestyle, predicts Ismail.

Researchers have agreed that more research in human clinical trials is necessary.

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“You must pay attention to extrapolation from mouse models, and you never know as long as you do not try it in a controlled human clinical trial,” noted Yankner. “But so far, the results are very encouraging.”

If future studies confirm these results, scientists say that routine blood tests could potentially detect lithium levels and identify people at risk.

“I hope that lithium will do something more fundamental than anti-amyloid or anti-mate therapies.”

Meanwhile, Yankner has warned of people who take lithium compounds “alone”.

“I hope that lithium will do something more fundamental than anti-amyloid or anti-mate therapies, not only reducing but reverse cognitive decline and improving the lives of patients,” he said.

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The study was supported by the National Institutes of Health, the Ludwig Family Foundation, the Glenn Foundation for Medical Research and the Aging Mind Foundation.