Zhen-Hua Zhao

Objectives: Parkinson’s disease (PD) patients frequently develop mild cognitive impairment (PD-MCI) and may progress to Parkinson’s disease dementia (PDD). Despite progress in understanding PD pathophysiology, reliable blood-based biomarkers for early detection and monitoring of cognitive decline remain lacking. This study aims to systematically evaluate and compare blood-based protein biomarkers for cognitive impairment in PD through a network meta-analysis (NMA). Methods: A systematic search was conducted across PubMed, Embase, Web of Science, Scopus, and the Cochrane Library from database inception to January 23, 2025, to identify studies investigating blood protein biomarkers for cognitive impairment in PD patients. Studies comparing biomarker levels between PD patients with cognitive impairment (PD-CI) and those with normal cognition (PD-NC) were included. Two independent reviewers extracted data, and risk of bias was assessed using the Newcastle-Ottawa Scale (NOS). A frequentist NMA was performed using Stata 15.0 with a random-effects model to estimate standardized mean differences (SMD) and 95% confidence intervals (CI). Results: A total of 47 studies were included, encompassing biomarkers from five functional categories: metabolic function, neuronal function, inflammatory and immune functions, blood and vascular functions, and others. Key findings demonstrated significant alterations in several biomarkers in PD-CI compared with PD-NC. Cystatin C (Cys C) levels were significantly elevated in PD-CI (SMD = 0.81, 95% CI: 0.32, 1.30). Glial cell line-derived neurotrophic factor (GDNF) levels were significantly reduced in PD-CI (SMD = −1.06, 95% CI: −1.71, −0.41). Neurofilament light chain (NfL) levels were significantly elevated in PD-CI (SMD = 0.72, 95% CI: 0.39, 1.05). Interleukin-6 (IL-6) levels were significantly higher in PD-CI (SMD = 0.20, 95% CI: 0.01, 0.92). Conclusion: This NMA identifies Cys C, GDNF, NfL, and IL-6 as promising blood-based biomarkers for detecting cognitive impairment in PD. These biomarkers reflect diverse pathological processes and hold potential for facilitating early diagnosis and monitoring, thereby improving patient management. Further research is warranted to validate these findings and explore their clinical utility. Systematic review registration: https://www.crd.york.ac.uk/PROSPERO/view/CRD42023488801 , Identifier: CRD42023488801.

Corrigendum: Evaluation of ferritin and TfR level in plasma neural-derived exosomes as potential markers of Parkinson's disease

Introduction: Early diagnosis of Parkinson’s disease (PD) remains challenging. It has been suggested that abnormal brain iron metabolism leads to excessive iron accumulation in PD, although the mechanism of iron deposition is not yet fully understood. Ferritin and transferrin receptor (TfR) are involved in iron metabolism, and the exosome pathway is one mechanism by which ferritin is transported and regulated. While the blood of healthy animals contains a plentiful supply of TfR positive exosomes, rare study has examined ferritin and TfR in plasma neural-derived exosomes in PD.Methods: Plasma exosomes were obtained from 43 patients with PD and 34 healthy controls. Neural-derived exosomes were isolated with anti-human L1CAM antibody immunoabsorption. Transmission electron microscopy and western blotting were used to identify the exosomes. ELISAs were used to quantify ferritin and TfR levels in plasma neural-derived exosomes of patients with PD and controls. Receivers operating characteristic (ROC) curves were applied to map the diagnostic accuracy of ferritin and TfR. Independent predictors of the disease were identified using logistic regression models.Results: Neural-derived exosomes exhibited the typical exosomal morphology and expressed the specific exosome marker CD63. Ferritin and TfR levels in plasma neural-derived exosomes were significantly higher in patients with PD than controls (406.46 ± 241.86 vs. 245.62 ± 165.47 ng/μg, P = 0.001 and 1728.94 ± 766.71 vs. 1153.92 ± 539.30 ng/μg, P < 0.001, respectively). There were significant positive correlations between ferritin and TfR levels in plasma neural-derived exosomes in control group, PD group and all the individuals (rs = 0.744, 0.700, and 0.752, respectively). The level of TfR was independently associated with the disease (adjusted odds ratio 1.002; 95% CI 1.000–1.003). ROC performances of ferritin, TfR, and their combination were moderate (0.730, 0.812, and 0.808, respectively). However, no relationship was found between the biomarkers and disease progression.Conclusion: It is hypothesized that ferritin and TfR in plasma neural-derived exosomes may be potential biomarkers for PD, and that they may participate in the mechanism of excessive iron deposition in PD.

Subarachnoid hemorrhage (SAH) is a serious disease caused by blood flow into the subarachnoid space due to rupture of blood vessels. All diseases that cause intracranial hemorrhage are the cause of subarachnoid hemorrhage. Among them, due to the particularity of intracranial blood vessels, intracranial blood vessels are more prone to aneurysms than other parts. Therefore, the incidence of aneurysmal subarachnoid hemorrhage (aSAH) is extremely high. The purpose of this article is to study the clinical treatment and prognosis analysis of aSAH patients. This article first summarizes the current status of SAH research at home and abroad and summarizes its potential value and significance. On this basis, an in-depth study of the clinical treatment of aSAH patients has been carried out. The physiological mechanism and clinical general differences of aSAH were studied and analyzed. This article systematically describes the application of CTP in the treatment and prognosis analysis of aSAH patients. Then, it will use a comparative analysis method, interdisciplinary method, and other research forms to carry out experimental research on the theme of this article. Research shows that rebleeding and blood sodium are the main factors for cerebral ischemia caused by aSAH.