Background: Human parvovirus B19 (B19V) infection is usually symptomless and occurs in the childhood. While in immunocompromised adults, B19V infection also presents various clinical symptoms due to the host's immune status. The classic symptoms include erythema, anemia, arthropathy, and edema, but neurological involvement is rare. Case Presentation: In this report, we present a case of B19V infection caused multiple organ dysfunction in a non-immunosuppressed adult. Metagenomic next-generation sequencing (mNGS) was used and successfully detected the pathogen in multiple types of samples, including blood, cerebrospinal fluid (CSF), and bronchoalveolar lavage fluid (BALF). The diagnosis was subsequently confirmed by polymerase chain reaction (PCR). He was treated with intravenous gamma globulin, resulting in a significant resolution of symptoms after 1 month. Conclusion: Multisystem involvement induced by B19V infection was found in this case report. mNGS performed great advantages in rapidly and accurately diagnosing B19V infection in multiple types of samples, which helps the timely adjustment of treatment and improves the prognosis.

Neurofilament light chain (NfL) was recently proposed as a promising blood biomarker for nervous system diseases, including Wilson's disease (WD). In this study, we investigated plasma NfL concentrations in patients with different types of WD and their correlations with clinical manifestations and brain atrophy. Seventy-five WD cases (54 neurological type, 21 hepatic type) and 27 age-matched healthy controls were included in this study. We compared plasma NfL concentrations between the different types and correlated them with Unified Wilson's Disease Rating Scale (UWDRS) scores. Patients were allocated to stable and unstable groups according to changes in UWDRS scores and clinical assessment. We compared the differences in plasma NfL concentrations between groups. Voxel-based morphometry (VBM) and FreeSurfer software were used to analyze MRI images. We investigated the correlation between plasma NfL concentrations and volume of gray matter, white matter, and several areas of interest in the brain MRI of 24 patients. Plasma NfL concentrations were significantly higher in neurological type WD than in hepatic type WD (8.16 vs. 3.19 pg/mL, p < 0.001). Plasma NfL concentrations were positively correlated with UWDRS scores (r = 0.291, p = 0.035) in patients with neurological type WD. Plasma NfL was significantly higher in unstable patients than in stable patients (10.74 vs. 7.23 pg/mL, p = 0.004). Significant negative associations were found between plasma NfL level and the volumes of total gray matter, bilateral caudate nucleus, putamen, and nucleus accumbens. Plasma NfL is valuable as a biomarker for neurological damage in patients with WD.

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Background: Penicillamine can trigger early neurological worsening in patients with Wilson’s disease (WD). We evaluated a very conservative regimen, starting at 125 mg/day and increasing the does stepwise at months 1, 3, and 6, combined with zinc, focusing on clinical outcomes, urinary copper, exchangeable copper (CuEXC), and plasma neurofilament light (NfL). Methods: We retrospectively analyzed 25 treatment-naïve patients with neurological WD who received penicillamine at 125 mg/day, with 125-mg/day increments at months 1, 3, and 6, plus zinc gluconate. Neurological status (UWDRS), 24-h urinary copper, CuEXC, and NfL were assessed at baseline and at 1, 3, 6, and 12 months. Neurological worsening was defined as an increase of more than 2 points in the UWDRS-N. Results: Nine patients (36%) experienced neurological worsened, all within the first 3 months. Patients who remained stable ( n = 16) showed progressive improvement in UWDRS scores and a sustained decline in CuEXC. Patients who experienced worsening had a blunted increase in urinary copper at 1 month and no significant reduction in CuEXC. ROC curve analysis showed that a 1-month urinary copper level above 473.85 μg/day was associated with a lower risk of worsening. Plasma NfL showed a mild, transient elevation in both groups at 1 month, followed by a decline only in the stable groups; however, between-group differences were not statistically significant. Conclusion: Neurological worsening remains frequent (36%) despite the ultra-low starting doses. A simple 1-month urinary copper threshold of 473.85 μg/day may help identify patients with more favorable outcomes. CuEXC and NfL changes parallel clinical courses but require larger validation.

Background: Cognitive impairment significantly impacts the quality of life in patients with neurodegenerative disorders, including Huntington's disease (HD), Parkinson's disease (PD), and Alzheimer's disease (AD). Objective: This study aims to assess the utility of MemTrax, a contemporary digital continuous recognition task platform originally developed for AD, as an effective tool for revealing cognitive and clinical motor impairments in HD and PD populations as aligned with respective disease staging. Methods: A total of 135 healthy controls, 131 HD, and 212 PD participants were included in the study. MemTrax metrics, recognition accuracy (MTx-%C), response time (MTx-RT), and a composite score (MTx-Cp) were correlated with clinical motor and cognition scales and disease staging. Results: MemTrax metrics showed stage-dependent declines in both HD and PD. In HD, both MTx-%C and MTx-Cp decreased significantly from pre-HD stage to stage 2 ( p < 0.001), showing negative correlations with motor impairment and cognitive scales. In PD, MTx-Cp declined across Hoehn and Yahr stages (1–4, p < 0.001), with strong negative correlations to Unified Parkinson's Disease Rating Scale Part III (UPDRS III) and positive links to Montreal Cognitive Assessment/Mini-Mental State Examination. Additionally, MTx-RT increased with disease progression and correlated positively with UPDRS III, indicating it could assess psychomotor slowing in PD ( p < 0.01). Conclusions: MemTrax effectively captures cognitive-motor decline in HD and PD. The responsivity of MemTrax to the severity of these disorders extends its utility beyond AD, positioning MemTrax performance as a cross-disease digital biomarker for early detection in neurodegenerative diseases.