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Missing Brain Element May Hold the Key to Stopping Alzheimer’s

Researchers at Harvard Medical School have unveiled groundbreaking findings: a lithium deficiency in the brain may act as a trigger for Alzheimer’s disease, while restoring the element could slow or even reverse its progression.

What Scientists Discovered

The team led by Professor Bruce Yankner found that in patients at the early stages of Alzheimer’s, lithium levels in the brain are significantly reduced. Moreover, lithium was shown to bind with amyloid plaques – protein deposits that damage neurons — rendering it unavailable for its protective function.

In mouse models of Alzheimer’s, supplementation with a specially designed compound – lithium orotate – produced remarkable results. Neurons retained their activity, pathological protein build-up was reduced, and memory and cognitive function improved substantially.

Why Lithium

Lithium has long been used as a treatment for bipolar disorder, but its role in brain health appears much broader. It helps regulate neural signaling and prevents cell death. A deficiency may set off a chain reaction that leads to the breakdown of neural connections and cognitive decline.

Therapeutic Prospects

Although results have so far been obtained only in animal models, researchers believe this discovery could redefine approaches to preventing and treating Alzheimer’s disease. The next step will be clinical trials in humans. If proven effective, this could mark the development of a new class of drugs capable of targeting the root cause of the disease rather than simply managing symptoms.

Why It Matters

Alzheimer’s disease is one of the most widespread and devastating neurodegenerative conditions globally. According to the World Health Organization, more than 55 million people live with dementia, with 10 million new cases diagnosed each year. The possibility of targeting the underlying cause of Alzheimer’s rather than its effects could mark a new era in global neuroscience and medicine.

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