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A groundbreaking study conducted by researchers at Cornell University has unveiled new insights into the function of a protein known as Eato, revealing its critical role in safeguarding the brain from neurodegenerative diseases such as Alzheimer's and Parkinson's.
The research, which utilized Drosophila fruit flies--organisms frequently employed in biological studies due to their genetic similarities to humans--shows that Eato not only protects neurons from destruction but also enhances the ability of phagocytes, the body's cellular cleaners, to remove damaged neurons efficiently.
According to the findings, when Eato is absent from neurons, those neurons do not perish independently. Instead, they trigger phagocytes to eliminate them, suggesting that Eato has a pivotal role in maintaining neuronal health. This discovery could pave the way for novel therapeutic strategies targeting neurodegenerative diseases.
Under normal circumstances, Eato conceals a fatty molecule called phosphatidylserine (PS) on the surface of healthy neurons. This molecule serves as a signal to phagocytes, indicating the neuron is ready for cleanup. When Eato is absent, PS prematurely exposes itself, causing phagocytes to mistakenly destroy healthy neurons alongside the damaged ones.
Eato is categorized as a member of the ABCA transporter protein family, which is essential for maintaining lipid balance within cells. Previous studies have linked several human ABCA transporters to Alzheimer's disease, indicating a significant connection between lipid transport and neurodegeneration.
Alzheimer's disease is recognized as the leading cause of dementia and ranks as the fifth most common cause of death among adults aged 65 and older. The financial burden of Alzheimer's care in the United States was approximately $305 billion in 2020, with projections suggesting this could exceed $1 trillion in the coming years. Similarly, Parkinson's disease incurs annual costs of approximately $51.9 billion, combining direct medical expenses and indirect costs such as lost wages and caregiving.
The research team has been investigating how phagocytes interact with neurons since 2018, focusing on the regulation of PS exposure. Their exploration of ABCA lipid transporters led them to uncover the unexpected dual role of Eato, which not only protects neurons but also aids phagocytes in identifying neurons marked for removal.
These findings are particularly striking, as they reveal that Eato functions differently in neurons and glial cells, yet suppresses PS exposure in both cell types. This discovery opens new avenues for potential treatments aimed at preventing the degeneration of healthy neurons in neurodegenerative conditions.
By deepening the understanding of proteins like Eato, researchers aim to develop methods to slow or even halt the progression of these challenging diseases. The current research emphasizes fundamental biological mechanisms, with hopes of translating these insights into therapeutic applications that could significantly impact the treatment of neurodegenerative diseases.
The study has been published in the journal Science Advances and highlights the collaborative efforts of various contributors from the Weill Institute for Cell and Molecular Biology at Cornell University.
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