NEFL antibody
- Known as:
- NEFL (anti-)
- Catalog number:
- orb66923
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- NEFL antibody
Related genes to: NEFL antibody
- Gene:
- NEFL NIH gene
- Name:
- neurofilament light
- Previous symbol:
- -
- Synonyms:
- NFL, CMT1F, CMT2E, NF68, PPP1R110
- Chromosome:
- 8p21.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2019-04-23
Related products to: NEFL antibody
Related articles to: NEFL antibody
- Multiple sclerosis lesions are dominated by clonally expanded CD8 T cells within an IFNγ-rich inflammatory microenvironment and neurons may be targets of these effector cells. However, the peptide antigens that CD8 T cells recognize on neurons are largely undefined. Neurons constitutively express low levels of HLA class I, and whether inflamed human neurons are competent to present a class I ligandome, what that ligandome contains, and whether presentation has functional consequences for autoreactive CD8 T cells remain open questions. Here we combine human iPSC-derived neural aggregates (HNAs), HLA class I immunoprecipitation coupled to LC-MS/MS immunopeptidomics, and microfluidic co-culture assays to map IFNγ-induced HLA class I presentation by neurons and to test antigen-specific cytotoxicity. IFNγ stimulation induced HLA class I upregulation in HNAs and enabled recovery of a canonical 8-12-mer class I ligandome enriched for 9-mers. Neuron-restricted expression of a synapsin-driven polyepitope cassette yielded presentation of defined exogenous 9-mer peptides on donor HLA class I molecules and, in the presence of IFNγ, elicited activation of autologous antigen-specific CD8 T cells and antigen-dependent neurite injury. Across four donors, comparative immunopeptidomics identified IFNγ-associated neural peptide repertoires that were distinct from those of matched fibroblasts and enriched for predicted HLA-B binding peptides. β2-microglobulin deletion ablated peptide recovery, and neuron-restricted reconstitution enabled identification of candidate neuron-derived peptides, including recurrent neurofilament light (NEFL)-derived peptides detected across donors. Together, these findings establish a human iPSC-derived platform for studying inflammatory neuronal HLA class I antigen presentation and antigen-dependent CD8 T cell engagement. - Source: PubMed
Publication date: 2026/06/17
Clarkson Benjamin DsPucci SusannaOverlee Brittany LShrestha Ramila BarunMangalaparthi Kiran KRaja RemyaShang PeiCurtis MarionPandey AkhileshHowe Charles L - Alzheimer's disease (AD) plasma and cerebrospinal fluid (CSF) proteomics can distinguish AD from cognitively normal controls, but the generalizability of machine learning performance and the recurrence of biological signals across datasets require cautious interpretation. We developed an explainable artificial intelligence framework spanning two fluids and four ADNI proteomic datasets, covering 2082 modality specific samples, all analysed internally within ADNI. Phase 1 analysed plasma using a 119 analyte NULISA and targeted UPENN panel (n = 727; 216 CE, 511 controls). Phase 2 extended the analysis to CSF using SOMAscan7k, TMT-MS and targeted SET2, with Elecsys Aβ42, Aβ40, total tau and p-tau181 as anchor biomarkers. Only SOMAscan was subject-independent relative to Phase 1 plasma; TMT-MS and SET2 overlapped with Phase 1 for 96.0% and 97.7% of subjects and therefore are not independent replication cohorts. Under subject-level splits with fold internal preprocessing, we compared Elastic Net, Explainable Boosting Machines and gradient boosted trees with SHAP-based explanations. Among the candidate pipelines reported in Table 3, we selected the pipeline with the highest held-out test ROC AUC for each platform; the selected values were 0.927 in plasma and 0.954-0.973 across the three CSF datasets. Because the same held out test performance was used for pipeline selection and headline reporting, these are optimistically selected single-holdout estimates, not unbiased estimates of generalizable or clinical performance. Explanations identified five recurring biological axes within ADNI: cholinergic (ACHE), tau/14-3-3 (YWHAG, YWHAZ, YWHAB, YWHAE), neuro-axonal (NEFL, NEFH), microglial/complement (CHIT1, SMOC1, CHI3L1, C7, CFH) and synaptic (NPTXR, NPTX2, DLG4, SYT5, VSNL1, ELAVL2). CSF analyses showed synaptic vesicle-cycle enrichment (q = 2 × 10), and CSF YWHAG correlated strongly with total tau (ρ = 0.87). Cross-fluid directional concordance was modest overall (54-57%) but increased to 73-80% among mapped analyte/protein rows reaching q < 0.05 in CSF. These findings provide hypothesis-generating, internally supported evidence within ADNI. Independent external cohorts with locked pipelines are required to evaluate generalizable performance and biological reproducibility; the overlapping TMT-MS and SET2 analyses should not be interpreted as independent replication. - Source: PubMed
Publication date: 2026/06/15
Donmez Turker BerkMohammedMansour - Parkinsonism encompasses Parkinson's disease (PD) and atypical syndromes including dementia with Lewy bodies (DLB), multiple system atrophy (MSA), progressive supranuclear palsy (PSP), and corticobasal syndrome (CBS), where early clinical differentiation remains challenging. This narrative review synthesizes evidence for two complementary biomarker families: alpha-synuclein seed amplification assays (α-synuclein SAA; including real-time quaking-induced conversion and protein misfolding cyclic amplification) as pathology-proximal markers of α-synuclein seeding and neurofilament light chain (NfL) as a marker of neuroaxonal injury and neurodegeneration burden. CSF α-synuclein SAA demonstrates high diagnostic accuracy for PD and DLB, but its performance is context-dependent, with reduced sensitivity in normosmic PD, some genetic subgroups (especially LRRK2-associated PD), very early or anatomically restricted Lewy pathology, and assay protocols not optimized for MSA strains. Recent biological classification frameworks, including SynNeurGe and neuronal α-synuclein disease integrated staging system (NSD-ISS), place SAA centrally in research definitions; however, clinical implementation requires a stewardship layer that preserves clinical judgment, recognizes S-negative genetic or atypical presentations, and avoids equating SAA positivity with a single clinical diagnosis. NfL reliably differentiates PD/DLB from atypical parkinsonian disorders, but interpretation requires age-, matrix-, and platform-specific cutoffs and attention to confounders, such as renal function, body mass index, diabetes, peripheral neuropathy, and vascular comorbidity. This review proposes pragmatic algorithms integrating pre-test probability, α-synuclein SAA, NfL, imaging, genetics, and patient communication. It emphasizes on how to explain positive, negative, and prodromal biomarker results without overdiagnosis, while acknowledging mixed pathologies and uncertain prognostic implications. - Source: PubMed
Publication date: 2026/06/15
Leclercq Vincent - Neuropsychiatric symptoms (NPSs) are prevalent in Alzheimer's disease (AD), yet their neurobiological etiology remains elusive. We investigated relationships between NPS subsyndromes, plasma neurofilament light chain (NFL), AD-vulnerable brain atrophy, and cognition. - Source: PubMed
Publication date: 2026/06/15
Wang Ya-YuZhu Huai-YuanMiao WeiWang Zhi-XinQin Jia-JiaSong Xiao-HanWang Yue-HuaSun Zhong-WuZhou XiaYu Xian-FengZhu Xiao-Qun - Relapsing-remitting multiple sclerosis (RRMS) is characterized by neuroaxonal damage, astrogliosis and inflammation. These mechanisms may already be active from early disease stages, underscoring the need for sensitive biomarkers capable of capturing treatment-related biological effects beyond conventional clinical measures. In this multicenter, ambispective, observational real-world study, the longitudinal effects of ozanimod on serum biomarkers were evaluated, during the first year of treatment in patients with low-to-moderate activity RRMS. Serum neurofilament light chain (sNfL), glial fibrillary acidic protein (sGFAP) and cytokines associated with immune activity (IFN-γ, IL-17, IL-6, IL-10, and IL-1β) were quantified at baseline, 6 months, and 12 months using an ultrasensitive single-molecule array (SIMOA). Ozanimod was associated with significant reductions in sNfLs and sGFAP at 12 months. Concomitantly, significant decreases in IFN-γ and IL-1β were observed. IL-17 levels remained unchanged in the overall cohort but decreased in patients with higher baseline IL-17 levels. These findings demonstrate coordinated modulation of biomarkers reflecting neuroaxonal damage, astroglial activation, and inflammatory activity under ozanimod treatment in early RRMS in real-world conditions. These results highlight the biological relevance of early intervention within a therapeutic window of opportunity and support the potential utility of serum biomarkers for monitoring biological treatment effects in clinical practice. - Source: PubMed
Publication date: 2026/05/29
Costa-Frossard LucienneBrieva LuisGarcía-Estévez Daniel ApolinarMartín-Martínez Jesús ManuelÁlvarez-Bravo GaryBlasco-Quílez María RosarioMeca-Lallana José ECalles-Hernández María CarmenRamo Tello CristinaMuñoz-Fernández CarmenBarbero David EnriqueLópez-Muñoz PabloPrieto González José MaríaCandeliere-Merlicco AntonioCarmona OlgaRiancho JavierSola-Valls NuriaCarcelén-Gadea MaríaBorrega LauraGascón-Giménez FranciscoVilanova DavidPérez XavierVillar Luisa María