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This review synthesizes the mechanisms by which C\/EBP\u03b2 modulates neuroinflammation and its potential as a therapeutic target. We conducted a comprehensive systematic review spanning January 1995 to June 2025, systematically querying Google Scholar and PubMed with the following keywords: neuroinflammation, inflammasome activation, C\/EBP\u03b2, therapeutic targeting, and neurodegenerative diseases. C\/EBP\u03b2 exists in three isoforms-LAP1, LAP2, and LIP-each with distinct functions in inflammasome activation. In Alzheimer\u2019s disease (AD), C\/EBP\u03b2 drives tau cleavage and A\u03b2 pathology through the AEP axis and exacerbates neuroinflammation by upregulating APOE4. In Parkinson\u2019s disease (PD), C\/EBP\u03b2 silencing reduces \u03b1-synuclein aggregation and dopaminergic neuron loss by suppressing the NLRP3 inflammasome. In Amyotrophic Lateral Sclerosis (ALS), C\/EBP\u03b2 is hypothesized to contribute to TDP-43-associated inflammasome activation, though this requires further validation. In Multiple Sclerosis (MS), C\/EBP\u03b2 may influence microglial activation and neuroinflammation, as shown in experimental autoimmune encephalomyelitis models. Modulators of the C\/EBP\u03b2-inflammasome axis include endogenous regulators like gut-derived metabolites and pharmacological interventions such as small-molecule inhibitors. Therapeutic strategies targeting C\/EBP\u03b2 hold promise for mitigating neuroinflammation and neurodegeneration, though challenges remain in achieving isoform-specific targeting and blood-brain barrier penetration. Future directions include CRISPR-based editing and biomarker development for personalized therapies.<\/jats:p>","DOI":"10.3389\/fimmu.2025.1656165","type":"journal-article","created":{"date-parts":[[2025,9,5]],"date-time":"2025-09-05T13:51:11Z","timestamp":1757080271000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":9,"title":["C\/EBP\u03b2 as a master regulator of inflammasome signaling in neurodegenerative diseases: mechanisms and therapeutic 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