Alzheimer's 'Three Major Pathologies' Controlled Simultaneously... Korean Researchers Uncover Therapeutic Mechanism [Reading Science]

Korea Brain Research Institute and Yonsei University Joint Research Team Confirms Efficacy of Insulin Receptor Inhibitor
Simultaneous Suppression of Inflammation, Amyloid, and Tau Proteins; Improvement in Cognitive Function Also Demonstrated

A domestic research team has identified a therapeutic mechanism that simultaneously regulates neuroinflammation, amyloid beta, and tau protein abnormalities—major causes of Alzheimer’s disease. They also demonstrated cognitive improvement effects in animal models, suggesting the possibility of a new strategy for dementia treatment.

The Korea Brain Research Institute (KBRI) announced on June 11 that the research team led by Heo Hyangsook, head of the AI-Based Brain Developmental Disorder Digital Medical Device Demonstration Support Project Group, together with Professor Seo Jinsu of Yonsei University, have elucidated the regulatory mechanism of the Alzheimer’s disease inhibitor ‘BMS-754807’, which acts on the insulin-like growth factor 1 receptor (IGF-1R).

Schematic diagram of the mechanism of action for improving Alzheimer's disease pathology by BMS-754807. The effect of BMS-754807, an IGF-1 receptor (IGF-1R) inhibitor, in alleviating brain inflammatory responses and major Alzheimer's disease pathologies (amyloid plaques, tau protein hyperphosphorylation) has been confirmed. Provided by the research team

Alzheimer’s disease is a representative degenerative brain disorder that results from a combination of chronic neuroinflammation, amyloid beta accumulation, and tau protein modification.

Suppressing Inflammation, Amyloid, and Tau Simultaneously

The research team administered BMS-754807 to human induced pluripotent stem cell (hiPSC)-derived cell models and Alzheimer’s animal models (5xFAD and PS19) to analyze its efficacy.

The results showed decreased production of inflammatory cytokines and suppressed excessive activation of microglia and astrocytes. Additionally, there was a significant reduction in amyloid plaque accumulation and tau protein hyperphosphorylation, which are key pathologies of Alzheimer’s disease.

Notably, the researchers also confirmed improvements in cognitive function along with recovery of synaptic function. Consistent results were observed in both human-derived cell models and animal models, supporting the therapeutic potential of this approach.

Heo Hyangsook stated, "Based on the mechanisms identified in this study, we plan to contribute to the development of future treatment strategies for neurological disorders."

Professor Seo Jinsu added, "The consistent effects observed in both human-derived cell models and animal models provide important evidence supporting the clinical applicability of this approach as an Alzheimer’s disease treatment strategy."

The results of this study were published in the latest issue of the international neuroscience journal, Journal of Neuroinflammation.

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