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<td><span style="font-family:Helvetica, sans-serif; font-size:20px;font-weight:bold;">Mind & Brain News -- ScienceDaily</span></td>
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<td><a href="https://www.sciencedaily.com/releases/2025/10/251010091559.htm" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">For the first time, scientists pinpoint brain cells linked to depression</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Oct 11th 2025, 01:56</div>
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<p>Scientists identified two types of brain cells, neurons and microglia, that are altered in people with depression. Through genomic mapping of post-mortem brain tissue, they found major differences in gene activity affecting mood and inflammation. The findings reinforce that depression has a clear biological foundation and open new doors for treatment development.</p>
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<td><a href="https://www.sciencedaily.com/releases/2025/10/251009033126.htm" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">Scientists discover brain circuit that can switch off chronic pain</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Oct 10th 2025, 06:16</div>
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<p>Scientists have pinpointed Y1 receptor neurons in the brain that can override chronic pain signals when survival instincts like hunger or fear take precedence. Acting like a neural switchboard, these cells balance pain with other biological needs. The research could pave the way for personalized treatments that target pain at its brain source—offering hope for millions living with long-term pain.</p>
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<p><strong>Forwarded by:<br />
Michael Reeder LCPC<br />
Baltimore, MD</strong></p>
<p><strong>This information is taken from free public RSS feeds published by each organization for the purpose of public distribution. Readers are linked back to the article content on each organization's website. This email is an unaffiliated unofficial redistribution of this freely provided content from the publishers. </strong></p>
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