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However, its role potentiating nigrostriatal neurodegeneration, particularly in response to mitochondrial dysfunction, remains unclear. Here, using histological, neurochemical and behavioral analyzes, we provide a complete characterization of a mouse model expressing the human LRRK2 G2019S mutation (hLRRK2*G2019S mice), in the context of aging and toxin\u2010induced parkinsonism. hLRRK2*G2019S young adult mice showed significant microglial activation and deficits in motor coordination, whereas aged transgenic displayed a hyperactive phenotype, despite the absence of evidence for nigrostriatal neurodegeneration in either young adult or aged animals. Furthermore, we assessed the vulnerability of LRRK2*G2019S transgenic mice to the chronic exposure to the mitochondrial complex I inhibitor 1\u2010methyl\u20104\u2010phenyl\u20101,2,3,6\u2010tetrahydropyridine (MPTP). Notably, no exacerbation of nigrostriatal neurodegeneration was observed in hLRRK2*G2019S mice, suggesting that this mutation does not increase sensitivity to mitochondrial stress. However, hLRRK2*G2019S MPTP\u2010treated mice present alterations, relative to WT counterparts, in the glial response induced by the neurotoxic treatment. These findings suggest that the G2019S mutation modulates the neuroimmune response but does not exacerbate nigrostriatal neurodegeneration in response to mitochondrial dysfunction. This highlights the mutation's complex role in PD pathophysiology.<\/jats:p>\n                  <jats:p>\n                    <jats:boxed-text content-type=\"graphic\" position=\"anchor\">\n                      <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/jnc70547-gra-0001-m.png\">\n                        <jats:alt-text>image<\/jats:alt-text>\n                      <\/jats:graphic>\n                    <\/jats:boxed-text>\n                  <\/jats:p>","DOI":"10.1111\/jnc.70547","type":"journal-article","created":{"date-parts":[[2026,9,9]],"date-time":"2026-09-09T09:16:33Z","timestamp":1788945393000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Neuroinflammatory and Motor Alterations in\n                    <scp>LRRK2<\/scp>\n                    *\n                    <scp>G2019S<\/scp>\n                    Transgenic Mice Without Enhanced Vulnerability to Aging or Chronic\n                    <scp>MPTP<\/scp>\n                    \u2010Induced Nigrostriatal Neurodegeneration"],"prefix":"10.1111","volume":"170","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8154-0265","authenticated-orcid":false,"given":"Roberto","family":"Garc\u00eda\u2010Swinburn","sequence":"first","affiliation":[{"name":"Instituto de Biomedicina de Sevilla (IBiS) Hospital Universitario Virgen del Roc\u00edo\/CSIC\/Universidad de Sevilla  Sevilla Spain"},{"name":"Departamento de Fisiolog\u00eda M\u00e9dica y Biof\u00edsica, Facultad de Medicina Universidad de Sevilla  Sevilla Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0004-3569-0555","authenticated-orcid":false,"given":"Laura","family":"Mor\u00f3n\u2010M\u00e1rquez","sequence":"additional","affiliation":[{"name":"Instituto de Biomedicina de Sevilla (IBiS) Hospital Universitario Virgen del 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