Dementia is a leading cause of disability, as well as the seventh leading cause of death globally.

By 2060, 14 million Americans are expected to have dementia.

Without new treatments, formal care for patients with dementia could exceed $1 trillion annually by 2060.

Dementia is a leading cause of disability and dependency among seniors globally. It is also the seventh leading cause of death. While the most common cause of dementia is Alzheimer’s disease (AD), which accounts for 60 percent to 80 percent of dementia cases, it is not the only one. Dozens of conditions can cause patients to experience mild cognitive impairment (MCI), followed by dementia.

Despite the different causes, the early signs and symptoms are often the same and include forgetfulness, getting lost even in familiar places, losing track of time, and problems finding words or following conversations. As the disease progresses, individuals may begin to notice significant personality changes, inappropriate behaviors, agitation, and less independence. By the final stages of dementia, individuals lose the ability to walk, communicate, and control bodily functions, meaning they need around-the-clock assistance with even basic activities.

Dementia is a tragedy on multiple levels that can place enormous strains on individuals as well as families.

Source: Annabel Podevyn (@alpn) / Unsplash

This level of care is often far too much for family members to manage, which leads them to seek outside assistance. According to a paper published in Nature Partner Journals Aging, the mean estimated costs for formal care per annum (in 2016) were $28,078, while informal care valued in terms of replacement cost and lost wages was $36,667 and $15,792, respectively. In total, that is $80,000 per patient per year.

While each instance of dementia is its own tragedy, its aggregate costs are astronomical because it affects an estimated 7 million Americans. The authors of the Nature Partner Journals Aging paper found that median costs for formal care in 2020 were $196 billion, while informal care valued in terms of replacement cost and lost wages were $450 billion and $305 billion, respectively. If rates remain static, 14 million Americans are expected to have dementia by 2060, with projected annual costs of $1.4 trillion for formal care. Annual informal care valued in terms of replacement cost and lost wages could be as high as $3.3 trillion and $2.2 trillion, respectively.

Though dementia is common, our understanding of how it develops and progresses remains frustratingly incomplete. This is true even of Alzheimer’s disease. Research has found that individuals who develop the disease experience buildups of amyloid plaques and tau protein tangles in their brains, but the reason is still not clear.

Available treatments for Alzheimer’s focus more on treating symptoms rather than addressing the underlying pathology of the disease. True, new medications like lecanemab and donanemab help patients with early-stage Alzheimer’s and may slow disease progression, but they are expensive and can cause significant side effects.

Given how many individuals and families are affected and will be affected by dementia, as well as how costly care will be, this is a problem that needs to be addressed from multiple angles. We most certainly need better treatments for Alzheimer’s, given its prevalence.

One potential treatment could be lithium.

THE BASICS

Lithium has been used within psychiatry for decades, and it has been approved for the treatment of acute mania and maintenance treatment for bipolar I disorder by the FDA. It is also an element that is found in drinking water and many foods at trace levels. The average person consumes about 0.6 to 3.1 mg of lithium per day—hundreds of times smaller than an effective therapeutic dose for the treatment of mania or bipolar disorder.

Lithium is also found throughout the human body, including the brain. This endogenous lithium has been overlooked by researchers for years, but a paper recently published in Nature by Aron and colleagues has found a significant association between reduced lithium concentrations in certain parts of the brain, the increased presence of amyloid plaques, and the incidence of MCI and Alzheimer’s in postmortem human brains. Their research indicates that amyloid plaques sequester lithium, which reduces its availability even in plaque-free parts of the brain.

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To further investigate the association, the team next explored “whether endogenous lithium homeostasis in the brain might be perturbed by Alzheimer’s disease pathology.” By studying mouse models, they found that Alzheimer’s does affect endogenous lithium levels, but more importantly, that the inverse is true. By feeding the mice a diet depleted of lithium, they observed accelerated deposition of amyloid plaque and tau protein accumulation.

The study’s findings indicate that lithium protects against some of the core symptoms of Alzheimer’s. It prevents memory loss by contributing to neuronal and synaptic health, helps to maintain the networks that connect neurons (particularly the integrity of myelin sheathing), and plays a role in the neuroimmune system by promoting healthy microglial functioning. As they write, “Lithium deficiency leads to a reactive pro-inflammatory state and impaired Aß [amyloid-beta protein] clearance.”

The researchers next explored whether lithium replacement therapy could influence Alzheimer’s pathology. Their research included more than a dozen Li salts, including both lithium carbonate (the Li compound used in psychiatry to treat bipolar disorder) and lithium orotate (C5H3LiN2O4). They found that lithium orotate “almost completely prevented” amyloid and tau accumulation, whereas lithium carbonate and other compounds had no significant effect. It also helped improve learning and spatial memory in mice with advanced amyloid pathology and reduced age-related neuroinflammation.

This evidence does not come out of the blue. Previous research (Chen and team, 2022) has suggested that patients who are prescribed lithium have a decreased risk of dementia, while elevated levels of lithium in Danish drinking water have been shown to have a negative association with the incidence of dementia (Kessing and team, 2017). However, what this study clarifies is that lithium orotate is not immediately sequestered by amyloid plaques, whereas other forms of lithium treatment are, suggesting that lithium orotate treatment may serve as a neuroprotective for healthy patients and that it could even reverse pathology.

One major concern is that high levels of lithium are toxic, particularly to the kidneys and thyroid. However, the initial study suggests that lithium orotate can be administered to patients in small enough doses to avoid toxicity while still having neuroprotective effects. The study’s authors report that clinical trials to determine safety and efficacy in humans are expected to begin soon.

References

Nandi, A. et al. (2024). Cost of care for Alzheimer’s disease and related dementias in the United States: 2016 to 2060. NPJ Aging. 2024 Feb 8;10(1):13. doi: 10.1038/s41514-024-00136-6.

Rajan, K. et al. (2022). Population estimate of people with clinical Alzheimer's disease and mild cognitive impairment in the United States (2020-2060). Alzheimers Dement. 2021 Dec;17(12):1966-1975. doi: 10.1002/alz.12362. Epub 2021 May 27.

Aron, L. et al. (2025). Lithium deficiency and the onset of Alzheimer's disease. Nature. 2025 Sep;645(8081):712-721. doi: 10.1038/s41586-025-09335-x. Epub 2025 Aug 6.

Chen, S. et al. (2022). Association between lithium use and the incidence of dementia and its subtypes: A retrospective cohort study. PLoS Med. 2022 Mar 17;19(3):e1003941. doi: 10.1371/journal.pmed.1003941.

Kessing, L.V. (2017). Association of Lithium in Drinking Water With the Incidence of Dementia. JAMA Psychiatry. 2017 Oct 1;74(10):1005-1010. doi: 10.1001/jamapsychiatry.2017.2362.