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Groundbreaking new approach to Alzheimer’s diagnosis and treatment

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By using this new imaging strategy, the group discovered that alterations in acetate and glucose metabolism were consistently observed in the AD mouse model and human Alzheimer’s patients. They were able to confirm that a strong correlation exists between the patient’s cognitive function and the PET signals of both 11C-acetate and 18F-FDG.

These results, the team said, suggest that acetate, previously considered an astrocyte-specific energy source, can facilitate reactive astrogliosis and contribute to the suppression of neuronal metabolism.

Dr Ryu Hoon, one of the researchers, explained: “By demonstrating that acetate not only acts as an energy source for astrocytes but also facilitates reactive astrogliosis, we suggested a new mechanism that induces reactive astrogliosis in brain diseases.”

Until now, amyloid beta (Aβ) has been suspected as the main cause of AD, and has been the focus of most dementia research.

Unfortunately, PET imaging targeting Aβ has had limitations in diagnosing patients, and drugs aimed at removing it as a target for AD treatment have so far all failed.

This study, the researchers said, offers a new possibility of using 11C-acetate and 18F-FDG PET imaging for early diagnosis of AD.

In addition, the newly discovered mechanism of reactive astrogliosis through acetate and MCT1 transporter suggests a new target for AD treatment.

Dr Lee concluded: “We confirmed a significant recovery when inhibiting MCT1, astrocyte-specific acetate transport, in an AD animal model. We expect MCT1 can be a new therapeutic target for AD.”

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