□ A research team led by Professor Jiwon Um from the Center for Synapse Diversity and Specificity at DGIST (President Kunwoo Lee) announced the world’s first discovery of a mechanism by which somatostatin, a brain neurotransmitter, directly regulates brain immune cells to alleviate Alzheimer’s disease. This study is expected to provide a strong foundation for repurposing existing medications for dementia treatment by shifting brain immune cells that worsen the condition into a “protective mode.”
□ Alzheimer's disease worsens as amyloid beta accumulates in the brain and the brain’s immune cells, microglia, become overactivated, leading to inflammation. During the early stages of the disease, microglia play a protective role by removing amyloid plaques, however, over time they become harmful, damaging brain synapses and driving inflammation.
The research team discovered that somatostatin prevents the overactivation of these immune cells and directly regulates them, restoring their role as the brain’s cleanup system. When somatostatin was applied to cultured microglia, their waste-engulfing (phagocytic) function improved significantly, and the secretion of inflammatory substances decreased. Specifically, the expression of brain-damaging inflammatory factors (IL-12) was effectively suppressed, whereas the anti-inflammatory factor (TGF-β) increased, thus completely converting brain immune cells into a gentle “protective state.”
□ Furthermore, the research team conducted an experiment to artificially increase the somatostatin levels in mice with Alzheimer’s disease. Consequently, the overactivation of immune cells that causes inflammation was successfully suppressed, and the accumulation of amyloid waste throughout the brain was substantially reduced. Notably, neurobehavioral analysis revealed that mice with elevated somatostatin levels exhibited a statistically significant improvement in long-term spatial memory, indicating meaningful cognitive improvement.
□ These findings are particularly significant as they could dramatically reduce the time required to develop treatments through drug repurposing using existing medications. The somatostatin receptor (SSTR) targeted in this study is already widely used in clinical settings, having received FDA approval for treating other conditions such as acromegaly. Earlier, clinical trials for Alzheimer’s disease demonstrated no clear effects owing to limitations in efficiently delivering drugs to the brain; however, this study identified the precise mechanism by which the treatment specifically targets microglia, introducing new possibilities for using existing drugs to treat dementia.
□ Professor Um emphasized, “This study demonstrates for the first time that somatostatin, a brain neurotransmitter, can directly regulate the state of immune cells to alleviate dementia pathology and improve memory function.” She further stated, “Previous clinical trials for dementia faced significant limitations. However, drugs already approved and used to treat other conditions now show new potential for application in treating dementia and neuroinflammation based on this newly discovered mechanism.”
□ This paper was jointly first-authored by Dr. Hyeji Jung and master’s student Gaeun Hyun from DGIST’s Center for Synapse Diversity and Specificity, and was published online on March 26, 2026 in the journal Brain, Behavior, and Immunity (ranked within the top 4% of JCR). Furthermore, this study was funded and supported by the Ministry of Science and ICT and the National Research Foundation of Korea.
Brain Behavior and Immunity
Somatostatin-induced modulation of microglial activity contributes to mitigating Alzheimer’s disease pathology
25-Apr-2026