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In these disorders, persistent danger signals, such as the aggregation of misfolded proteins, activate resident microglial cells, leading to a functional shift toward a detrimental, pro\u2010inflammatory phenotype. This damaging cycle is critically exacerbated by impaired Insulin\/Insulin\u2010like Growth Factor 1 signalling, which compromises neuronal mitochondrial homeostasis, decreases energy production, and severely diminishes synaptic plasticity, thereby establishing a self\u2010perpetuating cycle of metabolic disturbance and neuroinflammation. This review examines the burgeoning therapeutic potential of Glucagon\u2010Like Peptide\u20101 Receptor Agonists (GLP\u20101RAs), a class of drugs traditionally used to manage type 2 diabetes mellitus and obesity, as neuroprotective agents. We discuss mechanistic insights demonstrating how GLP\u20101RAs operate through a crucial dual action: effectively mitigating central insulin resistance and directly suppressing the multi\u2010faceted neuroinflammatory cascade. By activating specific neuronal and glial signalling pathways, GLP\u20101RAs are shown to restore mitochondrial function, increase neuronal resilience, and crucially, modulate adverse glial cell responses\u2014inhibiting the release of major pro\u2010inflammatory cytokines and significantly reducing cellular oxidative stress within the central nervous system. Clinical trials and comprehensive preclinical data, analysed through diverse experimental models of neurodegeneration, strongly support the translational potential relevance of these compounds. The accumulating evidence suggests that GLP\u20101RAs offer a promising, readily available therapeutic strategy to disrupt the core inflammatory and metabolic pathways common across many neurodegenerative conditions, warranting further investigation in large\u2010scale human trials.<\/jats:p>","DOI":"10.1111\/dom.70400","type":"journal-article","created":{"date-parts":[[2025,12,19]],"date-time":"2025-12-19T17:11:29Z","timestamp":1766164289000},"page":"1622-1637","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":16,"title":["Beyond diabetes and obesity:\n                    <scp>GLP<\/scp>\n                    \u20101 receptor agonists in disrupting the vicious cycle of metabolic dysfunction and neuroinflammation"],"prefix":"10.1111","volume":"28","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6144-8525","authenticated-orcid":false,"given":"Renata","family":"Spezani","sequence":"first","affiliation":[{"name":"Laboratory of Morphometry, Metabolism, and Cardiovascular Disease Institute of Biology, Biomedical Center, The University of the State of Rio de Janeiro  Rio de Janeiro Rio de Janeiro Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4134-7978","authenticated-orcid":false,"given":"Carlos A.","family":"Mandarim\u2010de\u2010Lacerda","sequence":"additional","affiliation":[{"name":"Laboratory of Morphometry, Metabolism, and Cardiovascular Disease Institute of Biology, Biomedical Center, The University of the State of Rio de Janeiro  Rio de Janeiro Rio de Janeiro 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