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
- Parkinson's disease (PD) is the second most common age-related neurodegenerative disorder, yet it remains unclear whether cortical architecture can reveal biologically distinct subtypes with distinct molecular and serum biomarker signatures. Two hundred PD patients and 121 healthy controls underwent structural MRI. Subject-specific cortical similarity networks were constructed using Morphometric INverse Divergence (MIND), and subtypes were identified with HYDRA. Spatial patterns were linked to regional gene expression from the Allen Human Brain Atlas through partial least squares regression, followed by functional and cell-type enrichment analyses. Serum neurofilament light chain (NfL) and glial fibrillary acidic protein (GFAP) were quantified using single-molecule array assays. No significant MIND differences emerged when PD patients were analysed as a single group. HYDRA identified two subtypes (ARI = 0.85) with divergent cortical organization that only partially overlapped with conventional motor phenotypes. Cluster 1 exhibited temporo-parietal MIND increases associated with synaptic and oligodendroglial signatures, without serum biomarker associations. Cluster 2 showed widespread fronto-cingulate MIND reductions enriched for mitochondrial, lysosomal, and proteostatic pathways, including the KEGG Parkinson's disease pathway, and these reductions correlated with higher serum NfL and GFAP. These findings reveal two biologically distinct PD subtypes with divergent molecular architecture and systemic neurodegeneration beyond conventional motor phenotyping. - Source: PubMed
Publication date: 2026/07/28
Bianco Maria GiovannaCalomino CamillaBonacci Maria CelesteCaligiuri Maria EugeniaCristiani Costanza MariaScaramuzzino LuanaBuonocore JolandaArcuri Pier PaoloQuattrone AldoQuattrone Andrea - Individuals with type 2 diabetes (T2D) have increased risk of acute myocardial infarction (AMI). Cardiovascular risk within T2D is heterogeneous and not fully explained by conventional risk factors, highlighting the need for improved biological risk stratification. - Source: PubMed
Publication date: 2026/08/11
Gurung Resham LalZheng HuiliTan Jia Le IvanWu HaoLiu SylviaDorajoo RajkumarLiu Jian-JunLim Su Chi - Subjective cognitive concerns frequently diverge from objective cognitive performance in cognitively unimpaired (CU) older adults, yet the neurobiological basis of this mismatch remains unclear. - Source: PubMed
Wan LuKang ChaeryonHarrison RaeSolis-Urra PatricioSewell Kelsey ROberlin Lauren EJain ShivangiHuang HaiqingGrove GeorgeKamboh M IlyasSutton Bradley PSnitz Beth EKramer Arthur FMcAuley EdwardBurns Jeffrey MHillman Charles HVidoni Eric DMarsland Anna LKarikari Thomas KMorris JillErickson Kirk I - The apolipoprotein E ε4 (APOE ε4) allele confers the greatest genetic risk for sporadic Alzheimer's disease (AD). - Source: PubMed
Publication date: 2026/08/07
Yang Ze-LinZhang CanTang ShiZhang Xin-YuHuang Liang-YuTan Lan Xu Wei - Late-onset unexplained epilepsy (LOUE) represents a substantial proportion of epilepsies with onset after 50 years and often manifests as temporal lobe epilepsy (LO-TLE). Although a link with Alzheimer disease (AD) has been suggested, only a subset of LO-TLE shows AD-related biomarkers, indicating biological heterogeneity. This study aims to characterize the cognitive and CSF phenotype of LO-TLE and compare it with healthy controls (HCs) and patients with mild cognitive impairment due to AD (MCI-AD). - Source: PubMed
Publication date: 2026/08/04
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