Harvard Medical School researchers confirm that depletion of lithium in the brain coincides with Alzheimers disease. Moreover, that simply replacing the metal with amyloid-evading salts could lead to the recovery and cure of Alzheimers disease.

Their analyses of human brain tissue, and a series of mouse experiments, published in Nature point to a consistent pattern: when lithium concentrations in the brain decline, memory loss tends to develop, as do neurological hallmarks of Alzheimer’s disease. The study also found evidence in mice that a specific type of lithium supplement undoes these neurological changes; rolls back memory loss; and restores the brain to a younger, healthier state.

Affecting an estimated 50+ million people worldwide, Alzheimer’s disease (AD) is distinguished by an array of observable brain abnormalities under the microscope like clumps of the protein amyloid-beta; neurofibrillary tangles of the protein tau; and the loss of a protective protein called REST.

Plying the brain the metals can be toxic, but the scientists at Harvard discovered a special class of lithium compounds that can actually evade the capture by amyloid-beta or plaque and restore the brain's memory.

While the German psychiatrist Alois Alzheimer suspected this from the off, it was his strict censor Dr. Oskar Fischer who warned “nature in the end is the ultimate pharmacy.”

“The majority of the Alzheimer’s research field has really focused on amyloid over the last 25 years,” says Melissa Murray, a neuroscientist at Mayo Clinic. “Initially, patients with increasing levels of amyloid were diagnosed with Alzheimers. In this way, the Alzheimer’s field became myopic. Then Mayo looked at the evolution of amyloid and tau simultaneously.” Murray continues:

Imagine looking at a tree. You can identify the tree’s natural experience with its environment by looking at it’s rings, patterns, and cross-sections. Similarly, by examining more than 3,600 postmortem brains, researchers at Mayo Clinic found that the progression of dysfunctional tau protein drives the cognitive decline and memory loss of Alzheimer’s disease.

However, Bruce Yankner, professor of genetics and neurology in the Blavatnik Institute at HMS, was the first to demonstrate that amyloid-beta was toxic back in the 1990s. So Yankner focused in on the lithium in the Harvard study. Does lithium have a baseline? How does it develop, progress or regress in relationship to AD? Again, that process required access to brain tissue, generally inaccessible in living people.

Alois Alzheimer originally used dyes to identify clumps of amyloid and tau proteins, and is credited with the first description of these microscopic changes in brain tissue. Alzheimer always performed post-mortem, but where Harvard stepped up was in replicating samples obtained from multiple brain banks—nationwide.

The lab partnered with the Rush Memory and Aging Project in Chicago, a bank of postmortem brain tissue donated by thousands of study participants across the full spectrum of cognitive health and disease. “Having that range was critical because trying to study the brain in the late stages of Alzheimer’s is like looking at a battlefield after a war,” says Yankner. “We needed to see the spectrum.”

Led by first author Liviu Aron, senior research associate in the Yankner Lab, the team used an advanced type of mass spectroscopy to measure trace levels of about 30 different metals in the brains and blood of cognitively healthy people; those in an early stage of dementia called mild cognitive impairment; and those with advanced Alzheimer’s. Yankner continues:

Lithium was the only metal that had markedly different levels across groups and changed at the earliest stages of memory loss. Its levels were high in the cognitively healthy donors, but greatly diminished in those with mild impairment or full-blown AD.

“Observing lithium levels in the brains of thousands of people who hadn’t received lithium treatment established a range or baseline for normal levels,” says Yankner, demonstrating that lithium plays an essential role in brain physiology. Moreover, the study coincided with lithium levels in the environment — particularly in drinking water — and crosschecked geographical populations studies which track and confirm the rise and fall of dementia rates across America.

“It’s the first time anyone’s shown that lithium exists at a natural level that’s biologically meaningful without giving it as a drug.” Then Yankner and colleagues confirmed what Dr. Alzheimer suspected all along. Lithium depletion isn’t merely a sign of Alzheimer’s disease. It could be Alzheimer's catalyst and cause.

Moreover, a large Danish study recently found that higher long-term lithium exposure in drinking water was associated with a lower incidence of dementia. The study, published in JAMA Psychiatry, analyzed data from over 800,000 individuals, comparing dementia rates across different levels of lithium exposure from drinking water. The presence of lithium in drinking water, and the possibility of artificially adding it, is a topic of ongoing political debate in the United States.

There are no established regulatory standards for lithium levels in drinking water in the United States at present. However, there is emerging evidence that suggests a potential link between PFAS or "forever chemicals" and an increased risk of Alzheimer's disease and other forms of dementia. While forever chemicals came into existence with the advent of Teflon in 1938, environmental contamination, waste and exploitation has been rife since the advent of the Industrial Revolution.

Though Alois Alzheimer coined the term Alzheimers in 1907, it was the work of a Czech academic, psychiatrist and neuropathologist Oskar Fischer — whose work came to bear in the Harvard study — who framed and qualified Alzheimer's disease through empirical discoveries.

In particular, a forensic exploration of neuritic plaque in 12 cases of senile dementia led Fischer to connect the cerebral plaque associated with Alzheimers disease to infection. “High consumption of aluminum from drinking water may be a risk factor for Alzheimer’s disease.” Where both agreed was that plaque was formed by microorganisms, extant from antiquity, forever lurking and looking for a host.