{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,24]],"date-time":"2026-08-24T05:19:00Z","timestamp":1787548740602,"version":"build-2736575974"},"reference-count":264,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,8,24]],"date-time":"2026-08-24T00:00:00Z","timestamp":1787529600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Pharmacol."],"abstract":"<jats:p>\n                    Parkinson\u2019s disease (PD) is traditionally described as a dopaminergic neurodegenerative disorder driven by \u03b1-synuclein aggregation and selective neuronal loss in the substantia nigra pars compacta. While this characterization captures the core clinical and pathological features, it does not fully explain disease initiation and progression. Converging evidence from human genetics, cellular and structural biology, and systems neuroscience now supports a unified framework in which PD results from the progressive erosion of mitochondrial resilience. Here, mitochondrial resilience denotes the capacity of neuronal mitochondrial networks to withstand stress and recover bioenergetic and cellular homeostasis through coordinated quality control, metabolic adaptation, and organelle communication. Rare, high-impact monogenic mutations in\n                    <jats:italic>PINK1<\/jats:italic>\n                    ,\n                    <jats:italic>PRKN<\/jats:italic>\n                    (encoding Parkin), PARK7 (\n                    <jats:italic>DJ-1)<\/jats:italic>\n                    ,\n                    <jats:italic>LRRK2<\/jats:italic>\n                    , and\n                    <jats:italic>SNCA<\/jats:italic>\n                    , along with common risk variants identified in genome-wide association studies, converge on interconnected pathways that govern mitochondrial quality control, bioenergetics, organelle dynamics, and cellular stress responses. These vulnerabilities are most pronounced in the highly energetic dopaminergic neurons of the substantia nigra, where sustained calcium cycling, high bioenergetic demand, and environmental stressors increase cellular susceptibility. Research has moved beyond early observations of respiratory chain impairment and oxidative stress to reveal context-specific disruptions in PINK1\/Parkin-mediated mitophagy, lysosomal trafficking, mitochondrial-derived vesicle dynamics, and neuroimmune signaling. This integrated framework reframes PD as a disorder of impaired cellular maintenance rather than solely a consequence of late-stage degenerative processes. It provides a translational shift from mechanism-based biomarkers to early detection of mitochondrial failure and supports therapeutic strategies aimed at restoring mitochondrial function and resilience, offering a direct route to disease-modifying neuroprotection in PD and potentially other neurodegenerative disorders.\n                  <\/jats:p>","DOI":"10.3389\/fphar.2026.1886917","type":"journal-article","created":{"date-parts":[[2026,8,24]],"date-time":"2026-08-24T04:23:17Z","timestamp":1787545397000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Mitochondrial resilience: a convergent framework for pathogenesis and neuroprotection in Parkinson\u2019s disease"],"prefix":"10.3389","volume":"17","author":[{"given":"Oscar","family":"Arias-Carri\u00f3n","sequence":"first","affiliation":[{"name":"Divisi\u00f3n de Neurociencias Cl\u00ednica, Instituto Nacional de Rehabilitaci\u00f3n Luis Guillermo Ibarra Ibarra","place":["Mexico City, Mexico"]},{"name":"Tecnologico de Monterrey, Escuela de Medicina y Ciencias de la Salud","place":["Mexico City, Mexico"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Magdalena","family":"Guerra-Crespo","sequence":"additional","affiliation":[{"name":"Laboratory of Regenerative Medicine, Department of Physiology, Faculty of Medicine, National Autonomous University of Mexico","place":["Mexico City, Mexico"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Luis O.","family":"Soto-Rojas","sequence":"additional","affiliation":[{"name":"Laboratorio de Investigaci\u00f3n en Neurociencias y Enfermedades Neurodegenerativas (LINEN), Carrera de M\u00e9dico Cirujano, Facultad de Estudios Superiores Iztacala, Universidad Nacional Aut\u00f3noma de M\u00e9xico","place":["Tlalnepantla, Mexico"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yeminia","family":"Valle","sequence":"additional","affiliation":[{"name":"Laboratorio de Neuroinmunobiolog\u00eda Molecular, Instituto de Neurociencias Traslacionales, CUCS, Universidad de Guadalajara","place":["Guadalajara, Mexico"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emmanuel","family":"Ortega-Robles","sequence":"additional","affiliation":[{"name":"Divisi\u00f3n de Neurociencias Cl\u00ednica, Instituto Nacional de Rehabilitaci\u00f3n Luis Guillermo Ibarra Ibarra","place":["Mexico City, Mexico"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel","family":"Ortu\u00f1o-Sahag\u00fan","sequence":"additional","affiliation":[{"name":"Laboratorio de Neuroinmunobiolog\u00eda Molecular, Instituto de Neurociencias Traslacionales, CUCS, Universidad de Guadalajara","place":["Guadalajara, Mexico"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,8,24]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"207","DOI":"10.1038\/nature20414","article-title":"Defects in trafficking bridge Parkinson\u2019s disease pathology and genetics","volume":"539","author":"Abeliovich","year":"2016","journal-title":"Nature"},{"key":"B2","doi-asserted-by":"publisher","first-page":"e21620","DOI":"10.1096\/fj.202100067R","article-title":"Mitochondrial fusion and fission: the fine-tune balance for cellular homeostasis","volume":"35","author":"Adebayo","year":"2021","journal-title":"FASEB J."},{"key":"B3","doi-asserted-by":"publisher","first-page":"1114","DOI":"10.1002\/mds.26605","article-title":"Neuropathological basis of nonmotor manifestations of Parkinson\u2019s disease","volume":"31","author":"Adler","year":"2016","journal-title":"Mov. 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