| Title: | Association of the Naples prognostic score with Parkinson disease risk: a prospective cohort study |
| Journal: | Frontiers in Aging Neuroscience |
| Published: | 30 Apr 2026 |
| DOI: | https://doi.org/10.3389/fnagi.2026.1809301 |
| URL: | http://dx.doi.org/10.3389/fnagi.2026.1809301 |
Publication 17789
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Abstract
The Naples prognostic score (NPS), derived from routine inflammatory and nutritional biomarkers, reflects systemic immune-metabolic status. Its prospective association with Parkinson disease (PD) risk has not been well established. We analyzed 317,035 UK Biobank participants recruited in 2006-2010 who were free of PD and malignancy at baseline and had complete NPS component data. NPS was derived from serum albumin, total cholesterol, neutrophil-to-lymphocyte ratio, and lymphocyte-to-monocyte ratio. Incident PD through 31 December 2022 was identified using a validated algorithm. Associations were examined using Cox proportional hazards models with multivariable adjustment. Over a median follow-up of 13.94 years, 2,298 participants (0.72%) developed PD. Higher NPS was significantly associated with increased PD risk. After multivariable adjustment, each 1-point increase in NPS corresponded to a 13% higher risk (Model 2 adjusted HR = 1.13, 95% CI: 1.07-1.19, p < 0.001). Compared with participants with NPS = 0, those with moderate to high NPS scores (2-4 points) had progressively elevated risks (NPS = 2: HR = 1.16, 95% CI: 1.03-1.31; NPS = 3: HR = 1.53, 95% CI: 1.29-1.82; NPS = 4: HR = 2.08, 95% CI: 1.21-3.58; all p < 0.05), showing a clear dose-response relationship (p for trend < 0.001). In this large prospective cohort, higher NPS was independently associated with increased PD risk. These findings support the potential role of integrated inflammatory-nutritional status in PD development and suggest that NPS may serve as a readily available marker for risk stratification.</p>
4 Authors
- Zhiqiang Xu
- Xiaoxiao Wang
- Gaiqing Yang
- Nan Li
1 Application
| Application ID | Title |
|---|---|
| 106707 | Causal effects of environmental, lifestyle, and genetic factors on chronic diseases. |
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