PET imaging of reactive astrocyte-neuron interaction reveals new insights into Alzheimer's disease pathology, offering a potential breakthrough in diagnosis and treatment. Recently, a team of South Korean scientists led by Director C. Justin LEE of the Center for Cognition and Sociality within th
South Korean researchers have discovered that reactive astrocytes, rather than amyloid-beta plaques, may be the main cause of Alzheimer’s disease. The team developed a new imaging technique using PET scans with radioactive acetate and glucose probes to visualize the interaction between astrocytes and neurons in Alzheimer’s patients. The researchers found that acetate, previously thought to be an energy source for astrocytes, can promote reactive astrogliosis and suppress neuronal metabolism.
Figure 1. Augmentation of acetate uptake, mediated by MCT1, facilitates Aβ-induced GABA release in reactive astrocyte. A. Blockade effect of MCT1 inhibitor on 14C-acetate uptake in primary cultured astrocytes. B. Blockade effect of Mct1 gene-silencing on 14C-acetate uptake in primary cultured astrocytes. C. Representative images displaying GFAP and MCT1 expressions in primary cultured astrocytes 48 hours after adenovirus treatment. D. The adenovirus effect on 14C-acetate uptake. E.
In this latest research, Lee’s team used positron emission tomography imaging with radioactive acetate and glucose probes to visualize the changes in neuronal metabolism in AD patients. Furthermore, they demonstrated that acetate, the main component of vinegar, is responsible for promoting reactive astrogliosis, which induces putrescine and GABA production and leads to dementia. First, the researchers demonstrated that reactive astrocytes excessively uptake acetate through elevated monocarboxylate transporter-1 in rodent models of both reactive astrogliosis and AD .
Dr. YUN Mijin commented, “Reactive astrocytes showed metabolic abnormalities that excessively uptake acetate compared to normal state. We found that the acetate plays an important role in promoting astrocytic inflammatory responses.”
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