<?xml version="1.0" encoding="utf-8" standalone="yes"?><rss version="2.0" xmlns:atom="http://www.w3.org/2005/Atom" xmlns:content="http://purl.org/rss/1.0/modules/content/"><channel><title>Neurodegeneration on Maragkakis Lab</title><link>http://maragkakislab.com/tags/neurodegeneration/</link><description>Recent content in Neurodegeneration on Maragkakis Lab</description><generator>Hugo</generator><language>en-us</language><lastBuildDate>Wed, 11 Jun 2025 00:00:00 +0000</lastBuildDate><atom:link href="http://maragkakislab.com/tags/neurodegeneration/index.xml" rel="self" type="application/rss+xml"/><item><title>Viral Infection Induces Alzheimer's Disease-Related Pathways and Senescence in iPSC-Derived Neuronal Models</title><link>http://maragkakislab.com/publications/2025-viral-infection-alzheimer-senescence/</link><pubDate>Wed, 11 Jun 2025 00:00:00 +0000</pubDate><guid>http://maragkakislab.com/publications/2025-viral-infection-alzheimer-senescence/</guid><description>&lt;h2 id="summary"&gt;Summary&lt;/h2&gt;
&lt;p&gt;Using iPSC-derived neurons and cerebral organoids, this study demonstrates that viral infections — including HSV-1 and tick-borne encephalitis virus — activate Alzheimer&amp;rsquo;s disease-related pathways and induce cellular senescence. The findings support a causal link between viral infection and neurodegeneration, suggesting that vaccination-based prevention of viral infections may reduce Alzheimer&amp;rsquo;s disease risk.&lt;/p&gt;</description></item><item><title>Mis-spliced transcripts generate de novo proteins in TDP-43-related ALS/FTD</title><link>http://maragkakislab.com/publications/2024-tdp43-mis-spliced-proteins/</link><pubDate>Fri, 26 Jan 2024 00:00:00 +0000</pubDate><guid>http://maragkakislab.com/publications/2024-tdp43-mis-spliced-proteins/</guid><description>&lt;h2 id="summary"&gt;Summary&lt;/h2&gt;
&lt;p&gt;This study demonstrates that loss of TDP-43 function leads to widespread cryptic splicing events that produce novel protein isoforms not normally expressed in healthy cells. These de novo proteins may contribute to the pathogenesis of ALS and FTD by triggering immune responses or impairing cellular functions.&lt;/p&gt;</description></item><item><title>Amyotrophic Lateral Sclerosis associated FUS mutation shortens mitochondria and induces neurotoxicity</title><link>http://maragkakislab.com/publications/2018-als-fus-mitochondria/</link><pubDate>Mon, 22 Oct 2018 00:00:00 +0000</pubDate><guid>http://maragkakislab.com/publications/2018-als-fus-mitochondria/</guid><description>&lt;h2 id="summary"&gt;Summary&lt;/h2&gt;
&lt;p&gt;This study shows that disease-associated FUS mutations cause mitochondrial shortening and fragmentation in neurons, leading to neurotoxicity. The findings connect FUS dysfunction to mitochondrial dynamics, providing a potential mechanism for neurodegeneration in ALS patients carrying FUS mutations.&lt;/p&gt;</description></item></channel></rss>