A new study published in Nature suggests that replenishing the brain’s natural lithium reserves could not only protect against Alzheimer’s disease but potentially reverse its debilitating effects as was witnessed in mice.

The study, led by geneticist Bruce Yankner of Harvard Medical School, found that “when lithium concentrations in the brain decline, memory loss tends to develop, as do neurological hallmarks of Alzheimer’s disease called amyloid plaques and tau tangles.” But the researchers discovered that a specific form of lithium supplement, lithium orotate, could undo this damage in mice, restoring their memory and reversing disease-related brain changes.

“This is groundbreaking,” said neuroscientist Ashley Bush from the University of Melbourne, who was not involved in the study, as quoted by Nature. “We only recently have the first disease-modifying drugs for Alzheimer’s disease. But they only target one thing: the amyloid plaques. This approach targets all the major pathologies of concern in the disease.”

Dementia, primarily Alzheimer’s, affects more than 55 million people worldwide. Current therapies, including the newly available anti-amyloid drugs, can only slow down the disease. As co-author Yankner put it, “They don’t stop it. They don’t restore function.”

“We don’t yet have the penicillin for Alzheimer’s,” he said.

The lithium clue

Historically used as a mood stabilizer and even once featured in the original formula of 7-Up, lithium has long intrigued scientists. People with bipolar disorder, for instance, showed slower brain aging when on lithium. Regions with trace lithium in drinking water also reported lower rates of dementia.

Yet clinical trials on lithium’s cognitive benefits yielded inconsistent results. Yankner’s team sought to understand why.

Their research marked a turning point: for the first time, they proved that “the metal is naturally present in the brain, where it has an important physiological role.” They also found that “lithium levels were lower in parts of the human brain affected by Alzheimer’s disease than in unaffected regions.”

Perhaps more crucially, the team discovered that in people with mild cognitive impairment (often a precursor to Alzheimer’s), lithium becomes trapped inside amyloid plaques — “leaving less available for essential brain functions.” The more the disease progressed, the more lithium was withdrawn from circulation.

Mouse models mirrored this disturbing trend. “A mouse with normal lithium levels in its brain had fewer amyloid plaques and tau tangles than did a mouse with lithium deficiency,” the authors reported. The cycle was self-reinforcing: “Less lithium in the brain leads to more amyloid, which leads to even less lithium.”

Breaking the cycle

When mice with Alzheimer’s-like symptoms were treated with low doses of lithium orotate, the results were stunning: “It reversed disease-related brain damage and restored the animals’ memory.”

With lithium orotate, the door to meaningful treatment, and perhaps prevention, may have opened wider.

The findings are still at the preclinical stage, and researchers caution that much remains to be tested in human trials.

Also read: Prolonged delay in REM sleep may signal higher risk of Alzheimer’s: Study