Lithium deficiency linked to onset of Alzheimer’s, study finds

Naturally occurring lithium in the brain may play a critical role in staving off Alzheimer’s disease (AD), found a new study, "Lithium deficiency and the onset of Alzheimer’s disease", published in Nature (nature.com) by Bruce A Yankner and colleagues from Harvard Medical School, Boston Children’s Hospital, and Rush University Medical Center.

Researchers analysed 27 metals in postmortem brain tissue from people with no cognitive impairment, mild cognitive impairment (MCI), and AD. Lithium was the only metal significantly reduced in the prefrontal cortex of both MCI and AD patients. The team found that amyloid plaques — a hallmark of AD — isolated lithium, reducing its availability to brain cells.

In mouse models, a lithium-deficient diet led to inflammation, sensory, motor, and cognitive impairments, and faster cognitive decline. Lithium orotate, a lithium salt that binds less to amyloid, reversed these effects, preserving memory and reducing brain inflammation without detectable kidney or thyroid toxicity.

The study also found correlations between higher cortical lithium levels and better memory performance in ageing individuals without dementia.

The findings point to lithium homeostasis as a potential early factor in Alzheimer’s development, with deficiency potentially triggering a self-reinforcing cycle of amyloid build-up and brain degeneration.

The authors suggest that low-dose lithium orotate supplementation could be explored as a preventive or therapeutic approach, though human trials will be needed to confirm safety and effectiveness.