Ask about this productRelated genes to: NRGN antibody
- Gene:
- NRGN NIH gene
- Name:
- neurogranin
- Previous symbol:
- -
- Synonyms:
- RC3
- Chromosome:
- 11q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 1996-07-17
- Date modifiied:
- 2016-10-05
Related products to: NRGN antibody
Related articles to: NRGN antibody
- Blood-based biomarkers for traumatic brain injury (TBI) are increasingly integrated into diagnostic algorithms, but their interpretation may be confounded by age-related neurological changes. This study quantified the relative effects of age and TBI on biomarker concentrations to determine whether age-related variation approaches or exceeds that associated with injury. - Source: PubMed
Mayes Katherine DVan Meter Timothy EMirshahi NazaninBoyd SallySandsmark DanielleRascovsky KatyaDiaz-Arrastia RamonWeppner JustinPeacock W FrankKuehl Damon R - Alzheimer's disease (AD) presents with substantial clinical and anatomical heterogeneity, including both typical amnestic and atypical variants such as posterior cortical atrophy and logopenic primary progressive aphasia. Although neurofibrillary tangle (NFT) burden is a defining pathological feature of AD, its regional distribution varies across clinical phenotypes, suggesting that selective neuronal vulnerability may shape disease presentation. However, the cellular and molecular determinants underlying this vulnerability remain incompletely understood. Here, we profiled single-nucleus transcriptomes across multiple brain regions, including hippocampal (CA1) and neocortical (superior temporal gyrus and occipital cortex) regions, from individuals with typical and atypical AD and healthy controls. Integrative analysis identified major cell classes and resolved diverse excitatory and inhibitory neuronal subpopulations that were reproducibly observed across regions and individuals. Using quasi-binomial regression models to assess compositional changes, we quantified subtype-specific vulnerability associated with AD pathology. We identified a distinct excitatory neuronal subpopulation characterized by NRGN and BEX1 expression, which showed reproducible depletion across multiple regions, with the strongest evidence in amnestic AD and in neocortical regions in lvPPA. This vulnerable population showed concordance with previously reported AD-associated excitatory neuron signatures, supporting a conserved transcriptional program of susceptibility. Genes enriched in this population were associated with chemical synaptic transmission and regulation of synaptic plasticity and formed interconnected networks in protein-protein interaction analyses. These findings suggest that intrinsic properties related to synaptic function may predispose specific neuronal populations to degeneration in AD. Together, our results define a conserved, transcriptionally distinct excitatory neuron subpopulation that is selectively vulnerable across AD phenotypes and brain regions. This work provides a framework for linking regional pathology to cell-type-specific susceptibility and highlights synaptic regulatory pathways as potential contributors to neuronal degeneration in Alzheimer's disease. - Source: PubMed
Publication date: 2026/04/01
Pereira Felipe LLew CarolineLi Song HRizzi LiaraSoloviev Alexander VPaes VitorBrooks Sara DSpina SalvatoreRexach Jessica ENewell Kathy LLeite Renata E PSeeley William WSuemoto Claudia KGhetti BernardinoMurray Melissa EGrinberg Lea T - Valproic acid (VPA) exposure is widely used to model autism spectrum disorder (ASD)-like phenotypes; however, the developmental timing and sex-specific molecular consequences of postnatal exposure remain incompletely understood. Disruptions in synaptogenesis and synaptic protein dynamics are considered central to the neurobiological underpinnings of ASD. This study investigated age- and sex-dependent behavioral and synaptic alterations following postnatal VPA administration during a critical developmental window (P30-P60). C57BL/6 female and male mice were exposed to a single intraperitoneal dose of VPA on postnatal day 14. Behavioral assessments included social interaction, open field, olfactory preference, and Morris water maze tests. Molecular analyses focused on the postsynaptic proteins Neurogranin (Nrgn) and PSD-95 (Dlg4) across the hippocampus, prefrontal cortex, and olfactory bulb. Postnatal VPA exposure produced age- and sex-dependent behavioral variability rather than uniform deficits. Males exhibited more pronounced modulation in locomotor and social parameters, whereas females showed relative resilience in spatial learning measures. In the hippocampus, VPA induced a significant increase in Nrgn mRNA and PSD-95 protein in 1-month-old males, suggesting temporally restricted synaptic remodeling during early maturation. These molecular alterations were region-specific and interaction-driven, with limited treatment effects observed in the prefrontal cortex and olfactory bulb. Importantly, protein levels were primarily influenced by age and sex rather than treatment alone, indicating tightly regulated developmental modulation rather than sustained synaptic loss. Collectively, these findings demonstrate that postnatal VPA exposure perturbs the temporal dynamics of synaptic maturation in a sex- and region-dependent manner, highlighting hippocampal vulnerability during adolescence. The results emphasize the importance of incorporating developmental stage and biological sex in mechanistic studies of ASD-related neuroplasticity. - Source: PubMed
Publication date: 2026/03/10
Tughan EmreDana HalimeYilmaz Ozge NurKocum FatmaDemiruz CicekDemirci EsraSener Elif Funda - This study elucidates the molecular pathogenesis of neurodevelopmental deficits in Chinese Allan-Herndon-Dudley syndrome (AHDS) patients caused by pathogenic SLC16A2 mutations. Genetic analysis of three Han Chinese patients with severe intellectual disability and global developmental delay identified two novel truncating mutations (c.1093del [p.A365Lfs35] and c.270_271del [p.G91Lfs28]) and a hemizygous de novo splice-site mutation (c.1026 + 1G > A). Structural modeling predicted that the c.1093del variant causes C-terminal truncation of transmembrane helix 12, which is likely to disrupt the T3-binding pocket by impairing the critical Arg445–His415 hydrogen bond. Functional studies confirmed significantly reduced SLC16A2 expression ( < 0.05) accompanied by dysregulated thyroid metabolism (increased and ; < 0.01) and downregulated neurodevelopmental genes ( and ; < 0.001). Mechanistically, MCT8 deficiency impaired cerebral thyroid hormone uptake, driving synaptic and axonal defects through dysregulation of both transcriptional and cytoskeletal programs: T3-dependent transcriptional suppression via inactivation of the promoter thyroid response element, and disruption of the signaling axis. These findings establish novel genotype-phenotype correlations in Chinese AHDS patients and provide a mechanistic framework for understanding the neurodevelopmental consequences of impaired thyroid hormone transport, with patient-derived iPSCs serving as a valuable resource for future therapeutic development. - Source: PubMed
Publication date: 2026/03/01
Sun XiaoangWang ChaoLin LonglongLan XiaopingWu ShengnanChen XuqinCai Cheng - encodes a sodium-citrate cotransporter implicated in early-onset epileptic encephalopathy and metabolic brain dysfunction, yet its developmental regulation and molecular context in the human brain remain incompletely defined. Leveraging human developmental transcriptomes from the Evo-Devo resource, we delineated tissue trajectories and network context for across the fetal-postnatal life. In the cerebrum, expression rises from late fetal stages to peak in the first postnatal year and then declines into adulthood, while cerebellar levels increase across the lifespan; liver shows a fetal decrease followed by sustained postnatal upregulation. A transcriptome-wide scan identified extensive positive and negative associations with , and a signed weighted gene co-expression network analysis (WGCNA) built on biweight midcorrelation placed in a large module. The module eigengene tracked brain maturation (Spearman rho = 0.802, = 8.62 × 10) and closely matched abundance (rho = 0.884, = 2.73 × 10), with a significant partial association after adjusting for developmental rank (rho = 0.672, = 6.17 × 10). Functional enrichment converged on oxidative phosphorylation and mitochondria. A force-directed subnetwork of the top intramodular members (|bicor| > 0.6) positioned adjacent to a densely connected nucleus including , , , , , , , and . Together, these results define a developmentally tuned, mitochondria-centered program that co-varies with in the human brain across the lifespan. It may provide insights to interrogate age-dependent phenotypes and therapeutic avenues for disorders involving citrate metabolism. - Source: PubMed
Publication date: 2026/01/30
Ferreira Bruna KlippelSchuck Patricia FernandaFerreira Gustavo CostaFreitas Hércules Rezende