Ask about this productRelated genes to: NMDAR1 antibody
- Gene:
- GRIN1 NIH gene
- Name:
- glutamate ionotropic receptor NMDA type subunit 1
- Previous symbol:
- NMDAR1
- Synonyms:
- GluN1
- Chromosome:
- 9q34.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-09-18
- Date modifiied:
- 2016-02-05
Related products to: NMDAR1 antibody
Related articles to: NMDAR1 antibody
- Various microRNAs (miRs) have long served as therapeutic targets for ischemic stroke, so we aimed to assess whether miR-92a-3p protects against cerebral ischemia and identify downstream targets in an animal model. For this purpose, rats were randomly divided into sham, middle cerebral artery occlusion (MCAO), miR-92a Agomir+MCAO, and miR-92a Antagomir+MCAO groups. Twenty-four hours before MCAO surgery, rno-miR-92a-3p Agomir or Antagomir (100µM) were injected into the right striatum of rats. Neurological deficit, infarction, blood-brain barrier (BBB), cerebral edema, oxidative stress and inflammation-related factors mRNA expression (GCH1, GRIN1, NOS1, and NOX1), and the activities of antioxidant enzymes (SOD and CAT), and GSSG in the piriform cortex-amygdala, striatum, and cortex areas were evaluated. Immunohistochemistry was used to count positive cells of TNF-α and p53, and H&E staining served to examine histological alterations. Significant reductions in neurological deficit, infarction volume, edema, and BBB permeability were observed in the miR-92a Agomir+MCAO group compared to the MCAO group. miR-92a Agomir significantly down-regulated the expression of GCH1, GRIN1, NOS1, NOX1, TNF-α, and p53. The activities of antioxidant enzymes were elevated following administration of miR-92a Agomir. Moreover, miR-92a Agomir could attenuate the GSSG levels. While the preconditioning paradigm limits direct clinical translation, these mechanistic insights provide a compelling rationale for evaluating delayed administration strategies in future translational studies. - Source: PubMed
Publication date: 2026/08/10
Ramdan MahmoudShahsavarani HoseinKhaksar SepidehMaleki Asghar AbbasiBigdeli Mohammad Reza - Hippocampal place cell activity represents an animal's location in space; yet, how hippocampal neuronal population dynamics change with spatial learning and the mechanisms underlying these activity changes, which drive allocentric navigation to a learned goal, are poorly understood. To address these questions, we performed calcium imaging with a novel wire-free waterproof miniaturized microscope to image the activity of large populations of hippocampal CA1 neurons during spatial learning of a two-dimensional navigational task, the Morris water maze. We followed the same cells during learning and were able to directly examine how each neuron in the ensemble, and the ensemble as a whole, changes its response properties. We found that neuronal spatial selectivity increased and population decoding of spatial location improved as mice learned to navigate to the goal. Viral CRISPR knock out of (encoding the essential GluN1 NMDA receptor subunit) in dorsal hippocampal neurons, dramatically reduced long-term potentiation in CA1. This manipulation also prevented the increase in spatial selectivity and improvement of population decoding with spatial learning and resulted in learning deficits in the Morris water maze. Together, our results show that dorsal hippocampus NMDAR-dependent synaptic plasticity is essential for the learning-dependent refinement of CA1 place selectivity and improvement in population decoding of space. - Source: PubMed
Publication date: 2026/07/15
Reshef RonenShahi MinaHo VictoriaOllivier MatthiasArac AhmetCohen ArielYamin DavidTran AmandaTjondropurnomo RuthKhakh Baljit SAharoni DanielO'Dell Thomas JGolshani Peyman - Amyloid-β accumulation, aberrant tau protein, neuroinflammation, and oxidative stress are some of the main pathogenic characteristics of Alzheimer's disease (AD), a degenerative illness characterized by cognitive deterioration. The majority of current AD therapies provide symptomatic alleviation with significant adverse effects, highlighting the urgent need for novel therapeutic approaches. - Source: PubMed
Publication date: 2026/07/22
Saini MayankHooda TanujDar Mohammad OvaisKumar SandeepKhatri RamchanderLather Amit - Background Cognitive symptoms after SARS-CoV-2 infection, often described as "brain fog," remain difficult to measure objectively and are biologically heterogeneous. DNA methylation may provide a stable, blood-accessible layer of information linking post-COVID immune remodeling, biological aging, and neuropsychiatric vulnerability. We re-analyzed GSE247869, a whole-blood Illumina MethylationEPIC dataset from individuals sampled six months after COVID-19 infection, to identify age-associated methylation signals with translational relevance. The present analysis was designed to characterize age-associated methylation within this post-COVID cohort, not to establish a COVID-19-specific signature or biological age acceleration. Methodology This was a cross-sectional analysis of a single post-COVID cohort, with 94 samples included in the age models and no COVID-19-negative comparator included in the analyzed model. Processed beta values were aligned to metadata, converted to M-values, and modeled at each cytosine-phosphate-guanine (CpG) using ordinary least squares with age and sex as predictors. Differentially methylated positions were corrected by Benjamini-Hochberg false discovery rate (FDR). CpGs were mapped to genes using robust annotation and Illumina manifest fallback. Gene-level signals were integrated using a multi-evidence prioritization score that incorporated statistical strength, effect size, multi-CpG support, direction consistency, known epigenetic-clock membership, and curated pathway membership. Results Within this cohort, the analysis identified 3,467 age-associated CpGs at FDR < 0.05, with an overall hypomethylation bias but focal hypermethylation at canonical aging loci. In total, 11 of 12 reference clock CpGs were recovered, including , , , , , and . The strongest exploratory signal was enrichment of glutamatergic/N-methyl-D-aspartate (NMDA) genes, including , , , , , and and had high integrated evidence scores and showed age-associated hypermethylation. The prioritized genes mapped interpretively to glutamatergic synapse, calcium signaling, and cAMP signaling pathways, although these complete KEGG pathways were not tested as formal enrichment categories. Conclusions This re-analysis recovered established age-associated CpGs and identified age-associated methylation enrichment near glutamatergic/NMDA genes within this post-COVID cohort. It cannot determine whether these signals are specific to COVID-19 infection, reflect accelerated biological aging, or relate to cognitive symptoms because no COVID-19-negative comparator or symptom-level cognitive phenotyping was included in the present analysis. The glutamatergic finding is hypothesis-generating, particularly because the curated set was small and no independent replication cohort was analyzed. Future longitudinal and case-control studies integrating / methylation with cognitive and inflammatory phenotyping are needed. Glutamatergic and calcium-signaling pathways may be evaluated in appropriately designed mechanistic and intervention studies, including but not limited to hypotheses related to the Cheung Glutamatergic Regimen, only after independent validation and careful safety evaluation. - Source: PubMed
Publication date: 2026/07/18
Cheung Ngo - Alzheimer's disease (AD) initiates with subtle neuroimmune alterations that precede overt synaptic loss and neuronal death, yet the early sequence linking Aβ exposure to glial activation remains incompletely understood. To capture early neuroimmune dynamics with greater physiological relevance, we employed primary mixed neuron-glia cultures derived from the hippocampi of postnatal day 1 (P1) mice. Unlike conventional coculture systems, these hippocampal mixed cultures preserve intrinsic neuron-astrocyte-microglia communication and recapitulate key features of the in vivo hippocampal microenvironment. Using this model, we investigated whether cannabidiol (CBD) modulates the initial pathogenic events triggered by Aβ during a 24h simultaneous cotreatment in cell culture. Aβ exposure induced robust hippocampal glial activation, oxidative stress, and elevated levels of proinflammatory mediators, particularly IL-1β, IL-6, and TNF-α. Notably, hippocampal synaptic and neurogenic markers (5HTA, Gria1, GRIN1, DCX, PSD-95) remained largely unaltered at this early stage, revealing a temporal dissociation in which glial-driven inflammation precedes synaptic dysfunction. CBD significantly attenuated inflammatory and oxidative responses and prevented Aβ-induced cellular damage, indicating engagement of endocannabinoid-related mechanisms that constrain early hippocampal glial reactivity. Although CBD did not fully normalize all glial alterations, it preserved hippocampal synaptic integrity and halted progression toward neuronal dysfunction. Together, these findings identify early hippocampal glial inflammation as a primary target of CBD and provide mechanistic insight into the temporal sequence linking Aβ exposure to neuroimmune activation. These results highlight early glial responses as a critical window for therapeutic intervention and support cannabinoid-based strategies to modulate the initial stages of Alzheimer's disease pathogenesis. - Source: PubMed
Salgado Karen Del Carmen Barbozade Albuquerque Ana Luiza SciandrettiPedrosa Tamiles Caroline FernandesCota Andressa Aparecida BatistaTalvani AndréOliveira Laser Antonio MachadoNogueira Katiane de Oliveira Pinto Coelho