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Alzheimer’s disease is a neurodegenerative disorder characterized by progressive memory loss, spatial disorientation, cognitive dysfunction, and behavioral changes. It is the most common form of dementia, affecting nearly 50 million people worldwide. One of the primary pathological hallmarks of Alzheimer’s disease is the progressive accumulation of amyloid-beta plaques in the brain. A new study in a mouse model of Alzheimer’s disease demonstrates that low-dose lithium may halt the progression of the disease by decreasing amyloid-beta plaque accumulation.
Lithium is a drug commonly used to treat bipolar disorder and drug-resistant depression. A microdose form of lithium, called NP03, consists of lithium encapsulated in a water-in-oil microemulsion. It is absorbed in the mouth to facilitate uptake and increase bioavailability. NP03 delivers doses of lithium that are up to 400 times lower than typical formulations.
The study involved transgenic mice that develop Alzheimer’s disease and its characteristic amyloid-beta plaque formation and cognitive impairments. The authors of the study gave the mice NP03 (40 micrograms of lithium per kilogram of body weight) five times a week for 12 weeks, to span the timeframe in which the mice would have amyloid-beta accumulation. They assessed the animals' ability to perform memory tasks and then measured levels of amyloid-beta and proinflammatory molecules in the animals' brains.
They found that NP03 improved cognitive performance, reduced amyloid-beta burden, and reduced markers of neuroinflammation and cellular oxidative stress in the mice. These findings suggest that a microdose lithium formulation may be beneficial in reducing amyloid-beta burden in the later stages of Alzheimer’s disease progression.