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Increasing clinical and experimental evidence, however, indicates that PD is a multisystem disease in which immune, metabolic, vascular, and peripheral nervous system dysfunction precede and shape motor circuit failure. Nonmotor manifestations, including olfactory impairment, sleep and autonomic disturbances, gastrointestinal dysfunction, and cognitive decline, often arise years before motor diagnosis, highlighting pathogenic mechanisms beyond dopamine deficiency alone. In this review, we synthesize evidence supporting the view that PD represents a disorder of chronic immunometabolic dysregulation rather than isolated neuronal loss. We focus on underestimated but high\u2010impact immunological control points that integrate central and peripheral disease mechanisms, including environmental and microbial immune priming, gut\u2013brain axis interactions, platelet\u2010mediated inflammatory signaling, amyloid\u2010\u03b2 (A\u03b2) as an innate immune peptide, immune checkpoint regulation via the PD\u20101\/PD\u2010L1 axis, and nicotinamide adenine dinucleotide (NAD\n                    <jats:sup>+<\/jats:sup>\n                    ) homeostasis governed by nicotinamide phosphoribosyltransferase (NAMPT). Recent pharmacological evidence further supports this framework, as metabolic interventions that improve systemic energy balance and reduce inflammation have also demonstrated neuroprotective effects in experimental models, reinforcing the concept that immunometabolic pathways are therapeutically actionable. Motor impairment in PD arises from basal ganglia network dysfunction, accompanied by pathological beta\u2010band synchronization, which is increasingly linked to neuroinflammation and metabolic stress. In parallel, platelet activation during inflammation and vascular injury releases amyloid precursor protein and A\u03b2, linking systemic immune activation to neurovascular signaling. Clinical observations from immune checkpoint inhibitor therapy demonstrate that disruption of PD\u20101\/PD\u2010L1 signaling can lead to Parkinsonism and neuroinflammatory syndromes, underscoring the importance of immune restraint in neural homeostasis. Finally, we highlight NAMPT\u2010dependent NAD\n                    <jats:sup>+<\/jats:sup>\n                    salvage as an important immunometabolic hub integrating energy metabolism, inflammation, and neuronal survival. Together, these findings support a unifying framework in which PD reflects failure of immunometabolic control across neural and peripheral systems, suggesting new avenues for disease\u2010modifying therapeutic strategies beyond symptomatic dopamine replacement.\n                  <\/jats:p>","DOI":"10.1155\/padi\/5349481","type":"journal-article","created":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T04:20:03Z","timestamp":1787026803000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Parkinson\u2019s Disease: Immunometabolic Control Points Across Neural, Vascular, and Peripheral Systems"],"prefix":"10.1155","volume":"2026","author":[{"ORCID":"https:\/\/orcid.org\/0009-0001-5388-4327","authenticated-orcid":false,"given":"Felix Y.","family":"Narvaez 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