FDA-Approved Drug Used for Dementia Treatment...DGIST "Tames Overactive Brain Immune Cells" [Reading Science]

Professor Jiwon Eom's Team at DGIST Identifies Somatostatin Mechanism for the First Time Globally
Confirmed to Improve Memory

The core mechanism by which a U.S. Food and Drug Administration (FDA)-approved drug can be used as a treatment for Alzheimer's disease has been identified for the first time in the world by a Korean research team. It was confirmed that the drug stops the overactivation of brain immune cells, which exacerbates dementia, and returns them to a 'cleaner mode,' even improving memory. This breakthrough is expected to dramatically shorten the development timeline for new drugs.

In Alzheimer's disease mice with increased somatostatin, microglia transitioned to an anti-inflammatory state, leading to reduced amyloid plaque accumulation and improved spatial memory. This result demonstrates that somatostatin is a key regulatory factor in alleviating dementia pathology. Provided by the research team

On April 6, a research team led by Professor Jiwon Eom of the Department of Brain Science at Daegu Gyeongbuk Institute of Science and Technology (DGIST) announced that they have, for the first time in the world, identified the principle by which somatostatin—a brain neurotransmitter—directly regulates microglia, the brain's immune cells, to alleviate Alzheimer's disease.

Alzheimer's disease worsens as amyloid-beta debris accumulates in the brain and microglia become excessively activated. In the early stages of the disease, these cells act as defenders by removing debris, but as the disease progresses, they turn into 'destroyers,' damaging synapses and triggering inflammation.

The research team confirmed that somatostatin converts these overactive microglia back to a neuroprotective state. In cell culture experiments, phagocytosis—the process of removing debris—was significantly increased, while the expression of the inflammatory factor IL-12 was inhibited and the anti-inflammatory factor TGF-β was increased. In other words, microglia reverted to their role as cleaners that protect the brain.

The effects were also evident in animal models of Alzheimer's disease. When somatostatin expression was increased, overactivation of microglia was suppressed and amyloid accumulation in the brain was significantly reduced. Notably, behavioral analyses showed a statistically significant improvement in long-term spatial memory, confirming the potential for actual cognitive function recovery.

Research team photo. From the left, Professor Jiwon Eom, Department of Brain Science, DGIST, Dr. Hyeji Jeong, Postdoctoral Researcher, and Ga Eun Hyun, Master's Student. Provided by DGIST

This study is particularly noteworthy because of the potential for repurposing existing FDA-approved drugs. The somatostatin receptor (SSTR) agonists used in the research are already being clinically applied to treat other conditions, such as acromegaly. Although previous dementia clinical trials showed limited results due to challenges in delivering the drug to the brain, the newly identified microglia-targeted mechanism greatly enhances the prospects for expanding its use as a dementia treatment.

Professor Jiwon Eom of DGIST stated, "This is the first time it has been demonstrated that somatostatin can directly regulate the immune cell state to alleviate dementia pathology and even improve memory. With a drug repurposing strategy that utilizes already approved drugs, we can significantly accelerate the development of treatments for dementia and neuroinflammation going forward."

This research was jointly led by Dr. Hyeji Jeong and master's student Ga Eun Hyun of DGIST as co-first authors, and was published online in the international journal 'Brain, Behavior, and Immunity' on March 26.

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