Neurological Sciences最新文献

{"title":"Association of fatigue and other non-motor and motor symptoms in Parkinson's disease.","authors":"Siming Jiang, Li Zhang","doi":"10.1007/s10072-026-09416-3","DOIUrl":"10.1007/s10072-026-09416-3","url":null,"abstract":"<p><strong>Background: </strong>Fatigue is a frequent and disabling non-motor symptom in Parkinson's disease (PD), which negatively affects patients' quality of life. The objective was to explore the association between fatigue and a comprehensive panel of non-motor and motor symptoms of PD.</p><p><strong>Methods: </strong>We conducted a cross-sectional study including 80 PD patients. Fatigue was assessed using the Fatigue Severity Scale. Demographic data, motor and non-motor symptoms were evaluated. Regression analyses were applied to analyse the impact of different variables on fatigue.</p><p><strong>Results: </strong>Fatigued patients exhibited longer disease duration, higher H&Y scale scores, more severe motor symptoms affecting activities of daily living (ADLs), and higher levels of anxiety, depression, and apathy. They also presented with more severe sleep disturbances, excessive daytime sleepiness, and frontal executive dysfunction. Multiple linear regression analysis revealed that fatigue severity was independently associated with excessive daytime sleepiness (ESS) and anxiety (HAMA). Logistic regression analysis identified female gender, higher Unified PD Rating Scale Part II (UPDRS-II) scores, higher ESS and HAMA scores as independent factors associated with the presence of fatigue; higher education level was associated with a lower risk of fatigue.</p><p><strong>Conclusion: </strong>Non-motor symptoms have a greater impact on PD-related fatigue than motor dysfunction per se, with excessive daytime sleepiness and anxiety being the most significant independent correlates. Female gender and severe motor symptoms affecting ADLs are also associated with an increased risk of fatigue in PD patients. Prospective interventional studies are warranted to verify the potential benefit of managing these non-motor comorbidities.</p>","PeriodicalId":19191,"journal":{"name":"Neurological Sciences","volume":"47 10","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149025667","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A multi-omics insight into the sex-specific burden of tobacco-associated neurodegeneration: trends, projections, and mechanistic clues from the TH gene.","authors":"Ying Xu, Qinwen Wang, Hongyu Tang, Guikai Ji, Runjuan Yang, Dongying Wu, Yaxing Gui","doi":"10.1007/s10072-026-09393-7","DOIUrl":"https://doi.org/10.1007/s10072-026-09393-7","url":null,"abstract":"<p><strong>Background: </strong>Tobacco exposure significantly influences neurological health, yet its specific associations with Parkinson's disease (PD) and Alzheimer's disease and other dementias (ADOD), including mechanisms, require clarification.</p><p><strong>Methods and materials: </strong>Using data from the Global Burden of Disease (GBD) 2021 study, multidimensional stratified comparisons of global PD and ADOD attributable to tobacco exposure were performed across dimensions including sex, socio-demographic index (SDI) quintiles, GBD sub-regions, and national levels. Furthermore, autoregressive integrated moving average and exponential smoothing models were incorporated to project trends until 2050. Bioinformatics analysis was conducted to identify key genes linking nicotine metabolism and sex differences.</p><p><strong>Results: </strong>Tobacco exposure exerted a negative modulatory effect on PD burden but increased ADOD risk. Marked sex-specific differences existed, with males more affected. Regional heterogeneity was pronounced: PD impact was strongest in East Asia, while ADOD burden was highest in high-SDI regions. Projections showed rising ASRs for males but a decline for females. Mechanistically, the TH gene was a key nexus connecting PD, nicotine pathways, and sex differences, potentially explaining the stronger effect in males.</p><p><strong>Conclusions: </strong>Tobacco exposure differentially influences PD and ADOD, with distinct patterns by sex and region. It is detrimental for ADOD but may negatively modulate PD. The burden is projected to increase over the next three decades with persistent sex disparities. The TH gene may provides a mechanistic clue for the sex-heterogeneous effect against PD.</p>","PeriodicalId":19191,"journal":{"name":"Neurological Sciences","volume":"47 10","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149016878","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Severe contrast-induced encephalopathy with permanent motor dysfunction following secondary ioversol exposure.","authors":"Jin Liu, Shao Luo, Lirong Zhu, Xianglin Zeng","doi":"10.1007/s10072-026-09417-2","DOIUrl":"10.1007/s10072-026-09417-2","url":null,"abstract":"","PeriodicalId":19191,"journal":{"name":"Neurological Sciences","volume":"47 10","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149017183","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Analysis of the off-target interaction of amyloid PET tracers with human brain sulfotransferases.","authors":"Ludovico Miccoli, Rosa Fullone, Stefano Delli Pizzi, Federica Tomaiuolo, Stefano L Sensi, Giuseppe Floresta, Alberto Granzotto","doi":"10.1007/s10072-026-09431-4","DOIUrl":"10.1007/s10072-026-09431-4","url":null,"abstract":"<p><strong>Background: </strong>Positron emission tomography (PET) tracers targeting amyloid-β (Aβ) are central to the diagnosis and staging of Alzheimer's disease (AD). However, growing evidence indicates that these tracers can engage off-target molecules, complicating signal interpretation. Sulfotransferases (SULTs) have been experimentally identified as binding partners of 11C-Pittsburgh Compound-B (PiB), but whether the clinically used fluorinated PiB derivatives interact with brain-expressed SULTs has not been explored.</p><p><strong>Objective: </strong>To assess whether PiB and its fluorinated derivatives flutemetamol and flutafuranol interact with the SULT isoforms expressed in the human brain, and to characterize the structural features of these interactions.</p><p><strong>Methods: </strong>We combined multi-omic transcriptomic profiling of the Genotype-Tissue Expression (GTEx) project and the Human Protein Atlas with molecular docking and molecular dynamics (MD) simulations to evaluate the structural interactions of SULT-tracer complexes.</p><p><strong>Results: </strong>SULT1A1, SULT1A3, and SULT4A1 were identified as the SULT isoforms predominantly expressed in the human brain, and all three are expressed in the cerebellum, the region used as a reference for Aβ PET signal normalization. Docking and MD simulations showed that all three tracers form energetically comparable complexes within the catalytic pockets of these isoforms, but their dynamic stability varied in an enzyme- and tracer-specific manner. PiB and flutemetamol were stably accommodated in SULT1A1, whereas PiB lost its initial pose in SULT4A1. Flutafuranol showed weaker binding to SULT1A1 but formed stable complexes in SULT1A3 and SULT4A1.</p><p><strong>Conclusions: </strong>These findings provide a structural framework for off-target interactions between Aβ PET tracers and brain SULTs and suggest that the intracellular enzymatic environment may contribute to variability in Aβ PET signals beyond fibrillar Aβ deposition.</p>","PeriodicalId":19191,"journal":{"name":"Neurological Sciences","volume":"47 10","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13624043/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149081681","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A multimodal model for clinically defined MCI integrating plasma biomarkers and brain microstructural features: a dual-cohort external validation study.","authors":"Jiayu Ke, Saiyare Xuekelati, Zhuoya Maimaitiwusiman, Buluhan Halan, Qihong Xu, Shuke Guo, Lei Xu, Hongmei Wang","doi":"10.1007/s10072-026-09378-6","DOIUrl":"10.1007/s10072-026-09378-6","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Objective: &lt;/strong&gt;Mild cognitive impairment (MCI) is clinically and etiologically heterogeneous. We aimed to develop and externally validate a multimodal model for distinguishing clinically defined MCI from normal cognition using plasma biomarkers and diffusion tensor imaging (DTI)-derived white-matter features.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;We analyzed 310 participants from a local discovery cohort (n = 153; 80 MCI and 73 cognitively normal [NC]) and an independent Alzheimer's Disease Neuroimaging Initiative phase 4 (ADNI4) validation cohort (n = 157; 68 MCI and 89 NC). Plasma phosphorylated tau 217 (p-tau217), neurofilament light chain (NFL), and glial fibrillary acidic protein (GFAP) were log-transformed and standardized using parameters estimated exclusively from NC participants in the local discovery cohort and then frozen for application to ADNI. Twenty-seven tract-level fractional anisotropy (FA) measures were considered as candidate imaging predictors. DTI feature selection used L1-penalized logistic regression with the 1-SE rule, with feature selection repeated within nested 10-fold cross-validation. Logistic regression (LR), support vector machine (SVM), random forest (RF), and XGBoost models were developed using local data, and the finalized pipelines were subsequently applied to ADNI4 without feature reselection, hyperparameter tuning, or recalibration.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Plasma p-tau217, NFL, and GFAP were higher in MCI than NC in both cohorts (all cohort-specific P ≤ 0.005). LASSO selected fornix (FX) and cingulum hippocampus (CGH) FA, and both features were retained in all 10 outer cross-validation folds. Nested internal AUCs ranged from 0.791 to 0.839. Under strict external validation, RF achieved the highest AUC of 0.829 (95% CI 0.762-0.889), followed by SVM with an AUC of 0.802 (95% CI 0.730-0.870), XGBoost with an AUC of 0.790 (95% CI 0.714-0.860), and LR with an AUC of 0.770 (95% CI 0.688-0.843). Relative to plasma biomarkers plus demographics, the full multimodal models significantly improved external discrimination across all four classifiers (all P ≤ 0.004). Improvements relative to DTI plus demographics were smaller and classifier-dependent; only RF showed a statistically significant increment (ΔAUC = 0.063, 95% CI 0.004-0.125; P = 0.036). RF had the lowest external Brier score (0.171). In the local cohort, lower FX and CGH FA remained associated with MCI after adjustment for available vascular and metabolic risk factors.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;A multimodal signature combining two selected DTI features with three prespecified plasma biomarkers and demographic covariates showed reproducible discrimination of clinically defined MCI across independent cohorts. The findings support further evaluation of this approach as an adjunctive MCI risk-stratification strategy but do not establish Alzheimer's disease (AD)-specific etiology or clinical readiness. Prospective validation incorporating","PeriodicalId":19191,"journal":{"name":"Neurological Sciences","volume":"47 10","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149002212","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to: Device aided therapies in Parkinson disease: an expert view on apomorphine.","authors":"Fabrizio Stocchi, Roberto Ceravolo, Carlo Colosimo, Maria Francesca De Pandis, Nicola Modugno, Manuela Pilleri, Alessandro Tessitore, Michele Tinazzi, Franco Valzania, Carmine Vitale, Roberta Zangaglia, Mario Zappia, Maurizio Zibetti, Angelo Antonini","doi":"10.1007/s10072-026-09407-4","DOIUrl":"10.1007/s10072-026-09407-4","url":null,"abstract":"","PeriodicalId":19191,"journal":{"name":"Neurological Sciences","volume":"47 10","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13585774/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148990431","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A scoping review of reversible cerebral encephalopathy syndromes following blood transfusion in the settings of anemia and clinical recommendations.","authors":"Hossam Tharwat Ali, Yazan Nouh, Abdullah Obadi, Ismail Habib, Khader Abutawahina, Abdulsalam Arebi, Mohannad Abd-Alhadi, Bahy El-Din Saied, Eman Shazly, Abdelrahman Nageh Ali Hafez","doi":"10.1007/s10072-026-09376-8","DOIUrl":"10.1007/s10072-026-09376-8","url":null,"abstract":"<p><strong>Background: </strong>Reversible cerebral encephalopathy syndromes (RCES), encompassing both posterior reversible encephalopathy syndrome (PRES) and reversible cerebral vasoconstriction syndrome (RCVS), represent a group of acute, neurotoxic neurological disorders that have been rarely linked to blood transfusion.</p><p><strong>Methods: </strong>A systematic search of PubMed, Web of Science, and Scopus using relevant keywords was carried out, followed by screening and extraction of only detailed cases of blood transfusion-induced PRES/RCVS until April 2025. Data on demographics, transfusion details (type, volume, and duration), clinical symptoms, imaging findings, and management details were extracted. Quality assessment using the Joanna Briggs Institute's (JBI) tool was performed.</p><p><strong>Results: </strong>Only 33 reports of 41patients were included, with a female majority (96.56%) and a mean (SD) age of 43.27 (14.53) years. The mean (SD) baseline and post-transfusion hemoglobin were 2.85 (1.23) and 9.55 (1.97) g/dL, respectively. The majority (95.12%) received packed red blood cells. The mean (SD) total volume transfused was 2100 (2560) ml. Headache (75.61%) was the most common symptom, followed by seizure (73.17%), visual disturbance (31.71%), and altered mental status (29.27%). Imaging studies revealed subcortical edema (46.34%), cortical infarcts (34.15%), subcortical infarcts (26.83%), and cortical edema (19.51%). PRES was diagnosed in 21 cases (51.22%), RCVS in nine cases (21.95%), and 11 (26.83%) had overlapping syndrome. The majority of cases (92.7%) were of high quality.</p><p><strong>Conclusions: </strong>In conclusion, anemia and its rapid correction via transfusion can precipitate RCES. Most cases have a good prognosis, and management is mainly supportive. Future studies need to guide preventive strategies and optimize patient outcomes.</p>","PeriodicalId":19191,"journal":{"name":"Neurological Sciences","volume":"47 10","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148983153","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Amyloid-beta-targeting monoclonal antibodies in early Alzheimer's disease: a cochrane review summary and appraisal for the neurological community.","authors":"Diogo Haddad Santos, Anderson Matheus Pereira da Silva","doi":"10.1007/s10072-026-09401-w","DOIUrl":"10.1007/s10072-026-09401-w","url":null,"abstract":"<p><strong>Background: </strong>Seven amyloid-beta-targeting monoclonal antibodies have been trialled in early Alzheimer's disease. They differ in epitope and in how much plaque they clear; only two have traditional approval. A 2026 Cochrane Review pooled all seven as one class. We ask what that average tells us about any one drug.</p><p><strong>Methods: </strong>We summarise the review in mild cognitive impairment or mild dementia due to Alzheimer's disease and report its estimates and certainty ratings unchanged. Our appraisal sits in a separate section and draws on the pivotal trials and regulatory assessments.</p><p><strong>Results: </strong>Seventeen trials (20,342 participants) were included. At 18 months the pooled standardised mean difference was -0.11 (95 % confidence interval -0.16 to -0.06) for cognition and -0.12 (-0.24 to 0.00) for dementia severity; three functional scales favoured treatment (0.09 to 0.23). Amyloid-related imaging abnormalities with oedema affected 119 versus 12 per 1,000 (risk ratio 10.02, 7.49 to 13.41). Four of the seven antibodies cleared no plaque or cleared it incompletely, so the pooled result cannot test whether clearance produces benefit. In the two approved agents dementia severity differed by 0.45 and 0.67 points, larger than the class average but below thresholds of clinical importance.</p><p><strong>Conclusions: </strong>The class average is not an estimate for any single agent. These antibodies clear amyloid and produce small differences on trial scales at 18 months, against a tenfold rise in amyloid-related oedema. Counselling should rest on agent-specific figures and a biomarker-confirmed diagnosis, and should weigh APOE ε4 genotype and antithrombotic use before the first infusion.</p>","PeriodicalId":19191,"journal":{"name":"Neurological Sciences","volume":"47 10","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13585809/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148990911","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Do not stop at the variant: a reversible cause of small-fiber neuropathy symptoms in an ATTRv carrier.","authors":"Gustavo Maximiano-Alves, Carolina Lavigne-Moreira, Matheus Compart Hemerly, Pedro Manoel Marques Garibaldi, Marcus Vinicius Simões, Wilson Marques","doi":"10.1007/s10072-026-09395-5","DOIUrl":"10.1007/s10072-026-09395-5","url":null,"abstract":"<p><strong>Background: </strong>Presymptomatic genetic testing in relatives of hereditary transthyretin amyloidosis (ATTRv) index cases enables early carrier identification and timely treatment, but a confirmed pathogenic variant carries the risk of premature diagnostic closure when new symptoms arise.</p><p><strong>Case presentation: </strong>A 25-year-old asymptomatic carrier of TTR: p.Val142Ile, whose father had neurological-predominant ATTRv, developed lower limb heaviness, burning pain, hyperesthesia, dysautonomia, and gastrointestinal symptoms. Cardiac work-up was unremarkable; electrochemical skin conductance testing was abnormal and gastric solid emptying scintigraphy was borderline. Before pursuing skin biopsy, a broad differential was investigated, revealing profoundly suppressed thyroid-stimulating hormone (TSH), elevated total triiodothyronine (T3), positive anti-thyroid peroxidase antibody (anti-TPO) and positive TSH receptor antibody (TRAb), confirming Graves' disease. Antithyroid treatment led to normalization of thyroid function and improvement of symptoms.</p><p><strong>Conclusion: </strong>Autoimmune thyroid disease may be an underrecognized, reversible cause of neuropathic symptoms. Systematic differential diagnosis is essential before attributing new symptoms to amyloidosis, preventing unnecessary initiation of disease-modifying therapy in patients with treatable alternative etiologies.</p>","PeriodicalId":19191,"journal":{"name":"Neurological Sciences","volume":"47 10","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148983278","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of age, BMI, and renal function adjustment on interpretation of serum NfL and GFAP in multiple sclerosis progression: a scoping review.","authors":"Aziza Shavkatovna Kadirova, Gulnora Kutpitdinovna Rakhmatullaeva, Javlon Jasur Ugli Salimjonov","doi":"10.1007/s10072-026-09408-3","DOIUrl":"10.1007/s10072-026-09408-3","url":null,"abstract":"<p><strong>Background: </strong>Despite achieving NEDA‑3, a substantial proportion of patients with multiple sclerosis (MS) accumulate disability through progression independent of relapse activity (PIRA). This scoping review evaluates serum neurofilament light chain (NfL) and glial fibrillary acidic protein (GFAP) in relation to disease activity and progression, with particular focus on the effects of age, BMI, and renal function on biomarker interpretation.</p><p><strong>Methods: </strong>The review followed PRISMA‑ScR guidelines (PubMed, Scopus, Web of Science, January 2016 - February 2026). Longitudinal studies (≥ 12 months) with multivariable adjustment were prioritised. Of 467 screened records, 367 were excluded; 100 full‑text articles were assessed. Of these, 36 were excluded. Sixty‑four publications were included; 34 original analytical studies formed the basis of the structured synthesis.</p><p><strong>Results: </strong>sNfL was consistently associated with acute inflammatory activity, whereas associations with progression were less consistent after adjustment for age and other covariates. sGFAP showed stronger associations with PIRA and disability progression in several longitudinal studies, although findings were heterogeneous. PIRA definitions and follow-up durations varied substantially, limiting direct comparability. Evidence regarding renal-function adjustment was limited and heterogeneous: adjustment attenuated the association between sGFAP and progression in one study, whereas associations remained evident in other studies accounting for renal function.</p><p><strong>Conclusions: </strong>Age, BMI, and renal function should be considered when interpreting circulating NfL and GFAP, particularly in studies of progression. The available evidence does not support universal biomarker cut-offs or uniform interpretation of PIRA-associated concentrations. Prospective studies with harmonised PIRA definitions, sufficiently long follow-up, and consistent confounder adjustment are needed.</p>","PeriodicalId":19191,"journal":{"name":"Neurological Sciences","volume":"47 10","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148990376","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}