A groundbreaking finding that could transform Alzheimer's disease diagnosis and treatment

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A team of scientists from South Korea, led by Director C. Justin LEE from the Institute for Basic Science's Center for Cognition and Sociality has achieved a significant breakthrough that has the potential to revolutionise the diagnosis and treatment of Alzheimer's Disease. The team has revealed a mechanism where astrocytes in the brain absorb high levels of acetate, transforming them into dangerous reactive astrocytes. They have also developed a new imaging technique that enables the direct observation of astrocyte-neuron interactions, leveraging this mechanism.

Alzheimer's Disease is a leading cause of dementia and is associated with neuroinflammation in the brain. Traditional neuroscience has long held that amyloid beta plaques are the cause, but treatments targeting these plaques have had limited success in treating or slowing the disease's progression.

Director C. Justin Lee's innovative hypothesis proposes that reactive astrocytes are the primary culprit in the development of Alzheimer's Disease. Reactive astrogliosis, a key feature of neuroinflammation in Alzheimer's Disease, frequently occurs prior to neuronal degeneration or demise. Lee's group has previously stated that therapeutic targets for Alzheimer's Disease can be reactive astrocytes and the monoamine oxidase B (MAO-B) enzyme found within these cells. They have also confirmed the existence of a urea cycle in astrocytes that promotes dementia.

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In their latest research, Lee's team used positron emission tomography (PET) imaging with radioactive acetate and glucose probes (11C-acetate and 18F-FDG) to observe the changes in neuronal metabolism in Alzheimer's Disease patients. The study is academically and clinically significant as it directly visualizes reactive astrocytes, which have recently been identified as a primary cause of Alzheimer's Disease.

Furthermore, the team demonstrated that acetate, the primary component of vinegar, promotes reactive astrogliosis, inducing putrescine and GABA production and leading to dementia. The researchers demonstrated in animal models of reactive astrogliosis and Alzheimer's disease that reactive astrocytes absorb an excessive amount of acetate due to the overexpression of monocarboxylate transporter-1 (MCT1). It was found that this elevated acetate uptake is linked to reactive astrogliosis and boosts aberrant astrocytic GABA synthesis when amyloid-beta, a well-known toxic protein in Alzheimer's Disease, is present.

Using PET imaging with 11C-acetate and 18F-FDG, the researchers were able to visualize the reactive astrocyte-induced acetate hypermetabolism and associated neuronal glucose hypometabolism in the brains with neuroinflammation and Alzheimer's Disease. When the scientists inhibited the reactive astrogliosis and expression of astrocytic MCT1 in the Alzheimer's Disease mouse model, they successfully reversed the metabolic alterations. Dr.YUN Mijin stated, "Compared to the normal state, reactive astrocytes displayed metabolic abnormalities that excessively absorbed acetate. We found that acetate plays a crucial role in promoting astrocytic inflammatory responses."

With the help of this new imaging technique, the team uncovered consistent alterations in acetate and glucose metabolism in both the mouse model of Alzheimer's Disease and human patients. The researchers confirmed a strong link between the cognitive abilities of patients and the PET signals of both 11C-acetate and 18F-FDG.These findings imply that acetate, which was previously considered as an energy source specific to astrocytes, can promote reactive astrogliosis and play a role in inhibiting neuronal metabolism.

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In summary, the recent breakthrough by Director C. Justin LEE and his team at the Center for Cognition and Sociality within the Institute for Basic Science in South Korea, provides a new understanding of the role of reactive astrocytes in Alzheimer's disease. By demonstrating that reactive astrogliosis induced by elevated levels of acetate can lead to neuroinflammation and cognitive decline, the team offers a new target for AD treatment.

The team's new imaging technique using PET imaging with 11C-acetate and 18F-FDG probes provides a non-invasive and accurate method of diagnosing AD by visualizing changes in neuronal metabolism. This new method may offer a more reliable and sensitive diagnosis of AD at an earlier stage, leading to more effective treatments.

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Moreover, the study sheds light on the role of reactive astrocytes in neuroinflammation, which is known to play a crucial role in Alzheimer's disease. The findings of this study suggest that reactive astrogliosis, characterized by the abnormal activation of astrocytes, contributes to neuronal degeneration and ultimately leads to dementia.

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The team's discovery of a mechanism by which astrocytes uptake elevated levels of acetates and turn into hazardous reactive astrocytes is a significant breakthrough. It provides new insights into the pathophysiology of Alzheimer's disease, challenging the traditional belief that amyloid beta plaques are the sole cause of the disease.

The team's new imaging technique, which enables direct observation of astrocyte-neuron interactions, is also an important step forward in the diagnosis and treatment of Alzheimer's disease. By visualizing the changes in neuronal metabolism in AD patients using PET imaging with radioactive acetate and glucose probes, the researchers were able to directly visualize reactive astrocytes, which Recently, they have been emphasised as a primary cause of Alzheimer's Disease.

The research also suggests that acetate, previously considered an astrocyte-specific energy source, can facilitate reactive astrogliosis and contribute to the suppression of neuronal metabolism. The discovery of this new mechanism suggests a new target for AD treatment, with the team proposing the astrocyte-specific acetate transport, MCT1, as a potential therapeutic target.

In conclusion, the study by Director C. Justin LEE and his team at the Center for Cognition and Sociality within the Institute for Basic Science in South Korea is a significant breakthrough in the diagnosis and treatment of Alzheimer's disease. Their findings challenge traditional beliefs about the cause of the disease and provide new insights into the role of reactive astrocytes in neuroinflammation. The team's new imaging technique and proposed therapeutic target offer new possibilities for the early diagnosis and treatment of AD.