by Raphael Wurm & Simone Salemme
Each month the eanNews editorial team reviews the scientific press for recently published papers of outstanding interest to neurologists. Below we present our selection for August 2026.
For our Research Paper of the Month, go here: Research Paper of the Month: Association of Sleep Duration with Alzheimer’s Disease and Cognition – eanNews
Amateur Soccer Heading Associated with Acute Increases in Neural Damage Biomarkers
This prospective, population-based case-control study assessed the association between heading the ball during a soccer game and blood biomarkers of neural damage measured immediately after in 302 amateur male players participating in organized matches. Heading exposure was present in 216 players (72%), averaging 2.0 (2.1) headers per player per match, with 48% exposed to high-impact headers (ball trajectories >20 m). Players exposed to heading showed significantly greater postmatch increases in protein S100B concentration (n = 299, P = .03; Cohen d = 0.29) compared with unexposed players. Furthermore, exposure to a higher frequency of headers demonstrated a dose-response relationship, associated with greater increases in both S100B (n = 299, P = .02; Cohen d = 0.07 per header) and p-tau217 concentration (n = 296, P = .01; Cohen d = 0.09 per header).
High-impact headers were similarly associated with significantly greater immediate increases in p-tau217 (n = 148, P = .03; Cohen d = 0.40) and S100B concentration (n = 149, P = .02; Cohen d = 0.43) relative to no exposure. All observed biomarker elevations normalized within 24 to 48 hours postmatch, and no other significant biomarker associations were identified. These findings indicate that even at the amateur-level, heading is acutely associated with transient reductions in neural integrity, supported by both dose-response and impact-intensity relationships.
Read the paper here: Amateur Soccer Heading and Acute Elevations in Blood-Based p-Tau217 and S100B | Neurology | JAMA Neurology | JAMA Network
Road Traffic Noise Exposure Associated with Increased Risk of Parkinson Disease
This Danish nationwide prospective cohort study investigated the association between long-term residential exposure to road traffic noise and incident Parkinson disease (PD) in 3,103,577 participants (mean age 50.9 years, 51.2% female). Over the follow-up period from 2000 to 2017, a total of 20,587 participants developed incident PD. In models adjusted for individual- and area-level sociodemographics, air pollution, and green space, road traffic noise exposure at the most exposed facade was associated with a higher risk of PD, yielding a hazard ratio (HR) of 1.03 (95% CI, 1.00–1.05) per interquartile increment of 11.5 dB. Noise exposure at the least exposed facade was similarly associated with PD risk (HR 1.04; 95% CI, 1.02–1.07 per interquartile increment of 8.9 dB).
A difference of ⪭10dB between noise levels at the most and least exposed facades (indicating access to a quiet facade) was associated with a reduction in PD risk across noise exposure levels above 50 dB at the primary facade. These findings indicate that long-term residential road traffic noise exposure represents a novel risk factor for PD. It should be noted that access to quiet surroundings mitigated this association, showing possible venues for prevention.
Read the paper here: Road Traffic Noise, Noise Difference Between Residential Facades, and Risk of Parkinson Disease | Neurology | JAMA Neurology | JAMA Network
Is Serum Neurofilament Light Chain Accurate Enough to Guide Multiple Sclerosis Care?
Serum neurofilament light chain (sNfL) is increasingly viewed as a minimally invasive biomarker of neuroaxonal injury in multiple sclerosis (MS), with potential value for detecting inflammatory disease activity and informing treatment decisions. However, an important practical question remains: is sNfL accurate enough to guide routine MS care as a standalone biomarker? Santana and colleagues addressed this question in a systematic review and meta-analysis evaluating the diagnostic performance of sNfL for MS disease activity, the methodological quality of the literature, and the optimal cutoff for predicting clinical relapses.
The authors searched PubMed/MEDLINE, Embase, and Scopus from inception to May 2026 and included studies of adults with MS in which sNfL was measured using single-molecule array (Simoa™). Eligible outcomes included clinical relapse, MRI activity, and no evidence of disease activity (NEDA-3). Overall, 28 studies comprising 11,213 patients were included. The authors reconstructed 2×2 contingency tables, performed hierarchical summary receiver operating characteristic analyses, conducted subgroup analyses by outcome and cutoff strategy, and used multi-cutoff modelling to estimate an optimal threshold for clinical relapse.
Diagnostic performance was consistently modest. Across analyses, pooled AUC values ranged from 0.61 to 0.71, below the prespecified threshold of 0.80 considered indicative of good clinical accuracy. Similar results were observed across outcome definitions and threshold approaches. The optimal cutoff for predicting clinical relapse was estimated at 10pg/mL, but performance remained limited, with sensitivity of 0.69, specificity of 0.65, and AUC of 0.72. Methodological concerns were also substantial: 14 studies were judged to have high risk of bias, mainly due to post hoc threshold selection, and the literature showed marked heterogeneity in disease-activity definitions, analytical methods, and cutoff strategies.
Overall, this study provides an important cautionary message for clinical translation. sNfL remains a biologically meaningful marker of neuroaxonal injury in MS, but current evidence does not support its use as a standalone biomarker for detecting inflammatory disease activity in routine care. Its greatest value may lie in multimodal predictive strategies that combine sNfL with clinical assessment, MRI measures, and complementary biomarkers, supported by prospective studies with standardised assays, harmonised disease-activity definitions, and externally validated thresholds.
Parkinson’s disease genetics across diverse ancestries: an observational genetic study of causal and risk variants with translational implications
Most Parkinson’s disease genetic research has historically focused on individuals of European ancestry, limiting understanding of how causal and risk variants are distributed across global populations. This gap is increasingly important as genetically informed therapies and clinical trials targeting pathways such as GBA1 and LRRK2 move closer to clinical translation. Lange and colleagues addressed this issue through a large multi-ancestry study within the Global Parkinson’s Genetics Program (GP2), aiming to characterise established causal variants and clinically relevant risk-associated variants across ancestrally diverse populations.
The study analysed GP2 release 11 data from 99,783 individuals, including 58,559 people with Parkinson’s disease and 41,224 controls. Participants came from 11 genetically inferred ancestry groups: African, African admixed, Ashkenazi Jewish, Latino and Indigenous people of the Americas, central Asian, complex admixture, east Asian, European, Finnish, Middle Eastern, and south Asian. The authors investigated causal and risk variants, including copy number variants, in established Parkinson’s disease and parkinsonism-associated genes, including GBA1, LRRK2, SNCA, VPS35, RAB32, PINK1, PRKN, PARK7, and several genes linked to atypical or complex parkinsonism.
Approximately 29% of the full sample came from under-represented populations, defined as non-European and non-Ashkenazi Jewish. Overall, 1,217 individuals with Parkinson’s disease carried a causal variant, corresponding to 2.1% of cases, but this proportion varied markedly by ancestry, from 0.4% among African individuals to 10.7% among individuals of Ashkenazi Jewish ancestry. Risk variants in GBA1 and LRRK2 were identified in 6,893 individuals with Parkinson’s disease, corresponding to 11.8% of cases, and in 3,578 controls. GBA1 risk variants were detected across all ancestries, although their frequency and variant spectra differed substantially. LRRK2 causal variants were most frequent in Ashkenazi Jewish and Middle Eastern groups, while LRRK2 risk variants were predominantly identified in east Asian individuals. Biallelic PRKN causal variants were identified across most ancestries, with the highest frequency in the Middle Eastern ancestry group.
Overall, this study provides an important equity-focused message for Parkinson’s disease genetics. Shared genetic contributors exist across ancestries, but ancestry-specific differences in variant frequency and spectrum are substantial and clinically relevant. As genetically stratified trials and targeted therapeutic approaches expand, inclusive genetic research will be essential to improve diagnostic accuracy, inform trial design, support genetic counselling, and ensure that emerging precision-medicine approaches are applicable and accessible to diverse populations worldwide.
Read the paper here: Parkinson’s disease genetics across diverse ancestries: an observational genetic study of causal and risk variants with translational implications – The Lancet Neurology
