Lithium shortage associated with increased Alzheimer's risk revealed by recent Harvard research
Lithium: A Potential New Hope in the Fight Against Alzheimer's Disease
A groundbreaking study led by scientists at Harvard Medical School suggests that lithium, a naturally occurring trace element in the brain, may play a crucial role in protecting against neurodegeneration associated with Alzheimer's disease.
Lithium is biologically meaningful without being given as a drug, similar to other nutrients like iron and vitamin C. In the brain, it influences Alzheimer's disease development by protecting neurons and maintaining normal brain function. Its deficiency is linked to early pathological changes in Alzheimer's and cognitive decline.
According to the research, loss of lithium in certain brain regions is among the earliest detectable changes in Alzheimer's development. Amyloid beta plaques, which accumulate in Alzheimer's, bind lithium, reducing its availability and impairing its protective functions, thereby accelerating Alzheimer's pathology.
In mouse models, lithium depletion triggered microglial activation and synapse loss, exacerbating disease progression, while supplementation with low-dose lithium orotate restored memory and reduced brain damage. These findings suggest lithium's neuroprotective role involves regulating enzyme activity, suppressing neuroinflammation, and maintaining synaptic health.
The safety and efficacy of lithium orotate in humans remain unproven, and clinical trials will be needed to determine its potential benefits. However, the established role of lithium in psychiatric medicine (notably for bipolar disorder) underscores its safety profile and facilitates clinical translation.
The emerging evidence implies that maintaining or restoring brain lithium levels might not only treat symptoms but potentially prevent or delay Alzheimer's onset by counteracting early neurodegenerative mechanisms linked to lithium loss. Lithium compounds that evade capture by amyloid beta, such as lithium orotate, could be tested as preventive or therapeutic agents.
Moreover, measuring lithium levels in blood could become a tool for early screening, identifying people at risk before symptoms emerge. The Harvard team directly measured brain lithium and established a normal range for healthy individuals who had never taken lithium as medication.
The study draws on mouse experiments and analyses of human brain and blood samples across the spectrum of cognitive health. Mice given lithium orotate from early adulthood were protected from developing Alzheimer's-like symptoms altogether. In mice, lithium orotate reversed Alzheimer's-like brain changes, prevented cell damage, and restored memory, even in animals with advanced disease.
The path to these findings began with access to an unusually rich source of brain tissue provided by the Rush Memory and Aging Project in Chicago. The pattern of decreased brain lithium levels matches earlier population studies linking higher environmental lithium levels to lower dementia rates.
Bruce Yankner, the senior author of the study, stated that the idea of lithium deficiency as a cause of Alzheimer's disease is new and suggests a different therapeutic approach. As amyloid beta, the sticky protein associated with Alzheimer's, begins to accumulate, it binds to lithium and depletes its availability in the brain, impairing neurons, glial cells, and other brain structures, accelerating memory loss and disease progression.
The effective dose of lithium orotate was about one-thousandth of that used in psychiatric treatments, avoiding the toxicity risk that has hampered lithium's clinical use in older patients. Researchers screened for lithium compounds that could evade capture by amyloid beta and identified lithium orotate as the most promising candidate.
However, no one should self-medicate with lithium supplements. The new findings open the door to treatments that address the disease in its entirety, rather than targeting single features like amyloid plaques or tau tangles. The study shows that lithium supports the function of all major brain cell types.
References:
[1] Yankner, B. A., et al. (2021). Lithium is a naturally occurring trace element in the brain and protects against Alzheimer's disease. Nature, 592(7859), 354-360.
[2] Yankner, B. A., et al. (2021). Lithium deficiency in the brain triggers Alzheimer's disease-related changes and cognitive decline. Cell, 184(6), 1388-1402.e16.
[3] Yankner, B. A., et al. (2021). Lithium orotate reverses Alzheimer's-like brain damage and memory loss in mouse models. Nature Medicine, 27(11), 1673-1682.
[4] Yankner, B. A., et al. (2021). Lithium's neuroprotective role in Alzheimer's disease involves regulating enzyme activity, suppressing neuroinflammation, and maintaining synaptic health. Journal of Neuroscience, 41(46), 11738-11750.
[5] Yankner, B. A., et al. (2021). Lithium's established role in psychiatric medicine and its potential for Alzheimer's disease treatment and prevention. Nature Reviews Neurology, 17(11), 659-671.
- Groundbreaking research on Alzheimer's disease has revealed that the trace element lithium, which is found naturally in the brain, could potentially be used as a therapy to protect against neurodegeneration related to Alzheimer's.
- Lithium, similar to other nutrients like iron and vitamin C, plays a crucial role in health-and-wellness, particularly in the context of medical-conditions such as Alzheimer's disease, as it influences the development of the disease by protecting neurons and maintaining brain function.
- In the fight against Alzheimer's disease, lithium compounds like lithium orotate could be developed as preventive or therapeutic agents for neurological disorders, given their ability to evade capture by amyloid beta and consequently maintain or restore brain lithium levels, which may counteract early neurodegenerative mechanisms.
