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<span class="word">Colchicine <span class="word">as <span class="word">a <span class="word">Repurposed <span class="word">NLRP3 <span class="word">Inflammasome <span class="word">Inhibitor <span class="word">in <span class="word">Amyotrophic <span class="word">Lateral <span class="word">Sclerosis: <span class="word">Mechanistic <span class="word">Rationale, <span class="word">Existing <span class="word">Clinical <span class="word">Evidence, <span class="word">and <span class="word">Proposal <span class="word">for <span class="word">a <span class="word">Precision <span class="word">Biomarker <span class="word">Trial

2026-03-18

Abstract excerpt

<h4>Background: </h4> Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterised by progressive motor neuron loss and neuroinflammmation. Current disease-modifying therapies provide only marginal benefit, and microglial NLRP3 inflammasome hyperactivation has emerged as a key pathological amplifier common to all ALS genetic and sporadic subtypes. Colchicine, an anti-inflammatory alkaloid...

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Literature Corpus work
4a50f7dc-2303-5576-a6dd-d8fc84b3dbda
DOI
10.20944/preprints202603.1495.v1
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<span class="word">Colchicine <span class="word">as <span class="word">a <span class="word">Repurposed <span class="word">NLRP3 <span class="word">Inflammasome <span class="word">Inhibitor <span class="word">in <span class="word">Amyotrophic <span class="word">Lateral <span class="word">Sclerosis: <span class="word">Mechanistic <span class="word">Rationale, <span class="word">Existing <span class="word">Clinical <span class="word">Evidence, <span class="word">and <span class="word">Proposal <sp…DOI 10.20944/preprints202603.1495.v1
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