Nefl polyclonal antibody
- Known as:
- Nefl pab (anti-)
- Catalog number:
- PAB12120
- Product Quantity:
- 50 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- Nefl polyclonal antibody
Related genes to: Nefl polyclonal 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 polyclonal antibody
Related articles to: Nefl polyclonal antibody
- Repetitive head impacts (RHIs) are associated with later-life neurodegeneration. Because soccer is the most widely played sport among youth worldwide, identifying early changes associated with RHI is important. - Source: PubMed
Publication date: 2026/06/01
Koerte Inga KWiegand Tim L TBonke Elena MSandmo Stian KKaufmann DavidSeer CarolineBetz Anja KDe Luca AlbertoSeitz-Holland JohannaMuehlmann MarcCente MartinElad DoronMonteiro Thiago SantosSchwarz-Mörtl BettinaGaubert MaloKaufmann ElisabethBonfert Michaela VHeinen FlorianLin Alexander PShenton Martha ETripodis YorghosBahr RoaldFilipcik PeterGooijers JolienLeemans AlexanderSochen NirSwinnen Stephan PPasternak Ofer - Alzheimer's disease shows prolonged prodromal stability before accelerating decline, yet molecular markers resolving this heterogeneity are limited. Using pseudo-progression analysis of 1.3 million SEA-AD single nuclei (84 donors), we identify a reproducible biphasic astrocytic trajectory anchored to prostaglandin D2 synthase (PTGDS), with a statistically resolved donor-level inflection (quadratic β₂ = -2.27, p = 0.006; vertex CPS 0.47). The same directional change is independently reproduced in external brain proteomics (ROSMAP and Banner; AD versus control p = 3.4 × 10⁻³), and the biphasic pattern reconciles previously conflicting CSF reports as stage-dependent. In ADNI CSF, downstream NEFL tracks cognitive decline strongly and LCN2 weakly, whereas PTGDS itself is tissue-restricted and not a stand-alone predictor. We propose, but do not establish, that post-inflection PTGDS attenuation accompanies LCN2-linked inflammation and NGFR suppression. These data position astrocytic PTGDS as a candidate stage marker, not a causal driver, of the compensatory-to-vulnerable shift in the aging brain - the astrocytic PTGDS inflection (CPS 0.47). - Source: PubMed
Publication date: 2026/06/10
Kim YoungOukHeo WooMyungPark Se JinKim YoungChulCho Ye EunLee Ye-WonKim JungYeon - Neurofilament light chain protein and glial fibrillary acidic protein have been proposed as potential blood biomarkers for multiple sclerosis. However, their diagnostic and prognostic values across different subtypes and disease activity patterns remain unclear. - Source: PubMed
Publication date: 2026/06/20
Yang ChengJiang ChenxiWang YirenHu YihengLi YunfeiZhou PingWang Youhua - 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, 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 BerkMansour Mohammed