Scientists have discovered a new method to combat Alzheimer's disease, revealing their latest breakthrough in research.

Korean researchers have identified a molecular mechanism that may regulate toxic amyloid beta, a protein closely associated with Alzheimer’s disease, potentially paving the way for new treatment strategies for sporadic cases of the disease. The Korean Institute for Health Industry Development announced this discovery on Monday, highlighting its significance for understanding the pathology of the disease and its future treatment, as reported by Korea Biomedical Review.

The study, led by An Ji-yin, a professor at the Sungkyunkwan University School of Medicine and published in the journal Nature Aging, examined the changes in expression of amyloid beta and EBP1, another protein linked to Alzheimer’s disease, in an animal model that closely mimics the condition observed in hospitalized patients.

The research demonstrated that decreased expression of EBP1 leads to the accumulation of toxic amyloid beta and cognitive dysfunction. By maintaining EBP1 levels and preserving its function, the team observed improvements in memory and cognitive abilities in mice that had the EBP1 gene removed.

The widely used mouse model for dementia research typically simulates the early stages of Alzheimer’s disease, which accounts for only about 5% of cases. However, sporadic Alzheimer’s disease, which arises due to aging rather than genetic mutations, constitutes the overwhelming majority of cases, creating a need for more advanced models to study this condition, the authors explained.

To address this gap, researchers investigated how EBP1 expression is specifically reduced in the aging brain and in patients with Alzheimer’s-type dementia. The results showed that in mice lacking EBP1, neuronal endotoxicity progressively worsens with age, leading to brain atrophy, neuroinflammation, and cognitive decline—symptoms that closely mirror sporadic Alzheimer’s disease in humans.

Further studies indicated that in the disease state, EBP1 undergoes abnormal cleavage, rendering it nonfunctional and, in turn, promoting the production of toxic intracellular amyloid beta. However, when researchers increased EBP1 activity in the Alzheimer's disease mouse model, the accumulation of amyloid beta significantly decreased, and learning and memory functions improved.

These findings underscore the potential of EBP1 as a target for future therapeutic approaches, according to the authors. Professor An emphasized that their research presents a new mouse model suitable for studying sporadic Alzheimer’s disease, which accounts for the majority of dementia cases. "This study identifies pathological mechanisms at the molecular and cellular levels, in animal models and patient tissues, and presents control mechanisms," she stated.

In subsequent research, the team aims to explore the mechanisms of clearing toxic proteins as a potential treatment strategy. Approximately 55 million people worldwide suffer from Alzheimer’s disease, and by 2050, the number of affected individuals is expected to reach 139 million. Current treatment methods focus on alleviating symptoms rather than addressing the disease itself, making breakthroughs in understanding its molecular mechanisms crucial for developing new therapeutic options.

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