GRIN2B (Glutamate Ionotropic Receptor NMDA Type Subunit 2B)

143B cell experiments and qRT-PCR validated findings. MFH-derived compounds, especially ellagic acid dihydrate, have multi-target anti-OS potential, laying a foundation for novel OS therapeutics.

In addition, suppressing or overexpressing METTL3, YTHDF1, and NMDAR2B correspondingly decreased or increased these effects, but modulation of NMDAR2B did not change the expression of METTL3/YTHDF1. rTMS can affect the polarization state of microglia and neuroinflammation by regulating the METTL3/NMDAR2B/NLRP3 signaling pathway, thereby improving NeuP.

P3, N=40, Recruiting, Meyer Children's Hospital IRCCS

This sensitization was also seen in the brainstems of mice receiving chronic morphine treatment and was mitigated by EGFR blockade. These findings suggest that EGFR-targeted cancer therapeutics may be repurposed to manage cancer pain and reduce opioid tolerance in patients with OSCC.

Perturbagen analysis nominated signature-reversing compounds across sexes, including histone deacetylase inhibitors, Aurora kinase inhibitors, microtubule-targeting agents such as vindesine, and multi-kinase inhibitors targeting VEGFR, PDGFR, FLT3, PI3K, and MTOR. Glioma grade comparisons reveal a shared neuronal-synaptic program accompanied by sex-specific transcriptional remodeling. These findings support sex-aware therapeutic strategies that pair modulation of neuron-glioma coupling with chromatin- or receptor tyrosine kinase/angiogenic-targeted agents, and they nominate biomarkers such as GLI1, MYOD1, GCGR, PRLHR, and HIST1H2BH for near-term validation.

Our results provide novel molecular insights regarding the roles of non-CNS cancer pathology and treatments in the brain related to calcium signaling and pro-survival/plasticity-related pathways. Our findings also point to potential treatments for cognitive effects of cancer.

These results contrast with prior reports of seizure-associated myelin modulation, indicating that seizure-induced myelin plasticity may not be a uniform feature across all models of absence seizures. Our findings indicate that such adaptations may depend on additional factors including seizure burden and timing, highlighting the need for further analysis to determine when and how myelin plasticity contributes to absence epilepsy.

Our findings demonstrate AD-specific increases in ES-GluN2B expression and a significant downregulation in PSA-NCAM levels, distinguishing AD from normal aging, potentially driven by Aβ-induced downregulation of biosynthetic enzymes ST8Sia4 and UDP-E. This underscores a potential link between PSA-NCAM expression and Aβ activity in AD, as well as possible therapeutic targets for AD intervention.

The RSV protects against CCH-induced neuronal damage by inhibiting apoptosis and enhancing synaptic plasticity. These findings highlight RSV's therapeutic potential for vascular cognitive impairment.

This study provides the first evidence linking NMDARs to IBC progression. Elevated expression and inhibition-sensitive aggressive phenotypes suggest NMDARs as potential biomarkers and therapeutic targets in IBC.

Additionally, Aβ suppressed PSA-NCAM biosynthetic enzymes ST8Sia4 and UDP-E linking Aβ to impaired polysialylation. These findings highlight distinct regulatory patterns of ES-GluN2B and PSA-NCAM in AD versus normal aging and support a model in which impaired PSA-NCAM buffering facilitates pathological ES-GluN2B signaling and plasticity loss in AD progression.

This study highlighted the regional distribution of NMDAR and Glx, underscoring their potential as diagnostic biomarkers for BrBM. Glutamine-based molecular imaging can noninvasively visualize the tumor microenvironment relevant to cancer neuroscience.