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                    <title><![CDATA[Cedars-Sinai Newsroom | Health Breakthroughs & Expert News]]></title>
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                    <lastBuildDate>Mon, 07 Sep 2026 18:12:12 +0200</lastBuildDate>
                    <pubDate>Mon, 25 Nov 2024 22:11:06 +0100</pubDate>
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                        <title><![CDATA[Cedars-Sinai Newsroom | Health Breakthroughs & Expert News]]></title>
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                        <title>Study: Immune Cells Protect Brain Against Delirium</title>
                        <link>https://www.cedars-sinai.org/newsroom/immune-cells-protect-brain-against-delirium/</link>
                        <guid>https://www.cedars-sinai.org/newsroom/immune-cells-protect-brain-against-delirium/</guid><pp:caseid>679289</pp:caseid><pp:subtitle>Cedars-Sinai Investigators Conclude Depletion of Cells Called Microglia Intensifies Delirium Symptoms, While Repopulating the Cells Relieves Symptoms</pp:subtitle><description><![CDATA[<p><span>Cedars-Sinai investigators have published a study in the peer-reviewed </span><a href="https://jneuroinflammation.biomedcentral.com/articles/10.1186/s12974-024-03260-y" target="_blank"><i><span>Journal of Neuroinflammation</span></i></a><i><span> </span></i><span>that found that immune cells in the brain can protect against delirium and could lead to new drug therapies to manage the condition.</span></p><p><span>Delirium causes confusion and behavior changes, affects millions of patients each year and can increase a patient’s risk of long-term neurological problems. It is common in hospitalized patients who are placed on ventilators to assist their breathing.<img class="image_resized image-style-align-right" style="width:200px;" src="https://content.presspage.com/uploads/2110/500_lahiri-shouri.lahiris.jpg?x=1732568660940" alt=" Shouri Lahiri, MD" width="200"></span></p><p><span>“Microglia, the resident immune cells in the brain, can be destructive to brain cells in some neurological diseases, but also can be protective,” said </span><a href="https://researchers.cedars-sinai.edu/Shouri.Lahiri" target="_blank"><span>Shouri Lahiri, MD</span></a><span>, director of the Neuroscience Critical Care Unit and director of Neurocritical Care Research in the Department of Neurology at Cedars-Sinai and senior author of the study. “While previous research has suggested that the action of microglia may cause or worsen delirium, we found that the opposite is true. When we depleted levels of microglia in laboratory animal experiments, delirium-associated brain changes and behaviors increased. And when we restored microglia levels to normal, the changes were almost completely reversed.”</span></p><p><span>Medications that activate neuron-protecting microglia could be one option for managing delirium. Investigators previously determined that a protein called interleukin-6 damages neurons, and future studies could clarify whether it or other proteins activate neuron-protecting microglia. Future research is also planned to help determine the conditions under which microglia can cause damage to neurons, said Lahiri, an associate professor in the departments of Neurology, Neurosurgery, and Biomedical Sciences.</span></p><p><i><span>First authors: Landon Scott, Kevin D. Winzey</span></i></p><p><i><span>Additional authors: Debbie Moreira, Catherine Bresee, Jean‐Philippe Vit, Warren G. Tourtellotte, S. Ananth Karumanchi, and Shouri Lahiri</span></i></p><p><i><span>Funding: F. Widjaja Foundation</span></i></p><p><span style="color:#dc1e34;"><i><span><strong>Follow&nbsp;</strong></span></i></span><a href="https://www.linkedin.com/company/cedars-sinai-academic-medicine/about/" target="_blank"><span style="color:#dc1e34;"><i><span><strong>Cedars-Sinai Academic Medicine</strong></span></i></span></a><span style="color:#dc1e34;"><i><span><strong>&nbsp;on LinkedIn for more on the latest basic science and clinical research from Cedars-Sinai.</strong></span></i></span></p>]]></description><category><![CDATA[Exclude,Research,Neuro,shouri-lahiri-1305724,Neuro Research]]></category>
            <pubDate>Wed, 27 Nov 2024 06:30:00 -0800</pubDate>
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