Alzheimer's & Lithium – Exciting New Research, But More Needed

A study by Bruce Yankner and colleagues at Harvard, published in Nature (August 2025), may represent a paradigm shift in understanding lithium's role in Alzheimer's disease (AD), demonstrating that lithium deficiency may be an early pathogenic event in AD.

The key findings were that:

1) Lithium is the only metal significantly reduced in the brains of individuals with mild cognitive impairment (MCI).

2) Among all metals analyzed, lithium was uniquely decreased in individuals with MCI, suggesting this occurs before clinical AD develops.

3) Lithium’s availability was further compromised in AD through amyloid-β sequestration, meaning amyloid plaques essentially trap lithium, making it unavailable to neurons.

4) Dietary lithium depletion accelerates AD pathology. 

When this team of researchers reduced brain cortical lithium by approximately 50% in wild-type and AD mouse models, they observed markedly increased amyloid-β deposition, phosphorylated-tau accumulation, pro-inflammatory microglial activation, synaptic and axonal loss, and myelin degradation – in other words, accelerated cognitive decline.

Lithium is an interesting chemical, from both basic science and medical science perspectives. It is a naturally occurring element that has been present in the environment since the Big Bang, making it one of the three primordial elements created during the formation of the galaxy. It is found in variable concentrations in rocks, soil, groundwater, and surface water worldwide. Lithium is naturally present in humans through dietary intake from food and water. Primary dietary sources include grains, vegetables, and drinking water.

While lithium has not been definitively classified as an essential nutrient, accumulating evidence suggests it may have important biological functions, as further demonstrated by the research of Yanker and colleagues.  Earlier laboratory animal studies show that lithium-deficient diets result in higher mortality rates and reproductive and behavioral abnormalities. In humans, low environmental lithium exposure has been associated with increased rates of suicide, homicide, and various psychiatric conditions.  

Lithium has a long history as a treatment for bipolar disorder. Interestingly, the results of multiple large-scale studies and meta-analyses have demonstrated that patients with bipolar disorder who receive lithium treatment have a lower incidence of Alzheimer's disease compared to those not receiving lithium. A UK retrospective cohort study of 29,618 patients found that lithium use was associated with reduced risk of all-cause dementia, AD, and vascular dementia. This finding is particularly significant given that bipolar disorder itself increases dementia risk approximately threefold compared to the general population. Lithium treatment appears to counteract this elevated baseline risk, potentially through its established neuroprotective mechanisms, including reduction of amyloid deposition and tau phosphorylation.

So, in summary, lithium shows potential neuroprotective effects in AD, with evidence suggesting it may reduce dementia risk and slow cognitive decline, though clinical efficacy remains incompletely established.

I advise against taking supplemental lithium unless prescribed by a physician. I urge you to continue to get the lithium you need from natural, unprocessed foods: potatoes, tomatoes, carrots, cabbage, and spinach are relatively rich sources. Also, rice, lentils, peas, nuts, seeds, citrus fruit, bananas, and grapes contain significant amounts of lithium.  

Finally, if you want to contribute to the advancement of medical science, consider clinical trials investigating lithium as a preventive and therapeutic strategy. https://clinicaltrials.gov/ is the place to check out possibilities. I predict there will be more trials coming this year and next.