{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,11]],"date-time":"2026-09-11T14:06:27Z","timestamp":1789135587015,"version":"build-2803163510"},"reference-count":70,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,11]],"date-time":"2026-09-11T00:00:00Z","timestamp":1789084800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100018587","name":"Yibin Science and Technology Bureau","doi-asserted-by":"publisher","award":["2024JC005"],"award-info":[{"award-number":["2024JC005"]}],"id":[{"id":"10.13039\/501100018587","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>Parkinson\u2019s disease (PD) is the second most prevalent neurodegenerative disorder worldwide, characterized by progressive loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) and the pathological accumulation of Lewy bodies composed predominantly of aggregated \u03b1-synuclein (\u03b1Syn). Despite decades of progress in genetics and neuropathology, the mechanisms driving disease initiation and progression remain incompletely understood, and no disease-modifying therapy has yet demonstrated conclusive efficacy. Neuroinflammation and metabolic dysfunction have emerged as two central and mechanistically intertwined pillars of PD pathogenesis. We propose an integrative model in which these processes function not merely in parallel, but as mutually reinforcing components of a self-amplifying pathological circuit, while acknowledging that this model remains to be fully validated and that alternative causal architectures are possible. This review systematically addresses the mechanistic coupling between neuroinflammation and metabolic dysregulation in PD, covering: (1) the molecular basis of innate immune activation via DAMPs, pattern recognition receptors, and inflammasome signaling; (2) microglial metabolic reprogramming and the NLRP3\/NF-\u03baB inflammatory axis; (3) \u03b1Syn-driven innate and adaptive immune responses; (4) mitochondrial dysfunction and oxidative stress as bidirectional amplifiers; (5) the gut-brain axis as a conduit for peripheral immunometabolic disruption; (6) the AMPK\/mTOR\/HIF-1\u03b1 molecular network integrating metabolism and inflammation; (7) sphingolipid metabolism and the GBA-lysosomal axis; and (8) translational evidence from animal models and randomized controlled trials. A concise section integrates key fluid biomarkers as clinical surrogates of the underlying mechanisms.<\/jats:p>","DOI":"10.3389\/fimmu.2026.1857394","type":"journal-article","created":{"date-parts":[[2026,9,11]],"date-time":"2026-09-11T13:09:36Z","timestamp":1789132176000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Neuroinflammation and metabolic reprogramming in Parkinson\u2019s disease"],"prefix":"10.3389","volume":"17","author":[{"given":"Yixin","family":"Fu","sequence":"first","affiliation":[{"name":"Department of Neurosurgery, The Second People\u2019s Hospital of Yibin","place":["Yibin, Sichuan, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jianghao","family":"Yu","sequence":"additional","affiliation":[{"name":"School of Medical Technology and Information Engineering, Zhejiang Chinese Medical University","place":["Hangzhou, Zhejiang, 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