{"id":8547,"date":"2025-02-10T12:47:43","date_gmt":"2025-02-10T20:47:43","guid":{"rendered":"https:\/\/keck.usc.edu\/news\/?p=8547"},"modified":"2025-04-18T16:37:40","modified_gmt":"2025-04-18T23:37:40","slug":"usc-led-study-finds-potential-new-drug-target-for-alzheimers-disease","status":"publish","type":"post","link":"https:\/\/keck.usc.edu\/news\/usc-led-study-finds-potential-new-drug-target-for-alzheimers-disease\/","title":{"rendered":"USC-led study finds potential new drug target for Alzheimer\u2019s disease"},"content":{"rendered":"\n \n \n\n\n\n\n\n\n\n
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USC-led study finds potential new drug target for Alzheimer\u2019s disease<\/h1>\n\n\n<\/div>\n \n \n
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Researchers used a combination of animal models, human brain tissue and molecular analysis to reveal a link between Alzheimer\u2019s disease and issues with cell function and cholesterol in the brain.<\/p>\n\n\n\n<\/div>\n \n

\n Zara Abrams<\/span>\n \n February 10, 2025<\/span>\n <\/div>\n \n \n
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A team of researchers from the Keck School of Medicine of USC has unlocked the details of a cellular pathway that triggers cellular inflammation and aging and is linked to Alzheimer\u2019s disease, particularly among those who carry the APOE4 genetic risk. They have also found a way to return cells to a healthy state, revealing a new potential approach to treatment. The study, the culmination of a decade of research on a protein known as ATP-binding cassette transporter A1 (ABCA1), was just published in the journal Molecular Neurodegeneration<\/a>.<\/p>\n

Past research found that a shortage of HDL cholesterol (or \u201cgood cholesterol) in the brain raises a person\u2019s risk for Alzheimer\u2019s disease. That risk is related to problems with ABCA1, which produces HDL when working properly. But fixing those problems requires understanding the exact biological mechanisms at play\u2014and those details have long eluded researchers, who faced an apparent paradox. In brains affected by Alzheimer\u2019s disease, ABCA1 molecules increased, but their activity decreased.<\/p>\n

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