Analysis of NMDA Receptor-mediated Excitotoxicity in Stroke

N-methyl-D-aspartate receptors (NMDARs) play a key role in excitotoxicity induced by ischemic stroke. Although NMDAR is associated with excitotoxicity associated with ischemic stroke, it remains a double-edged sword. Activation of NMDAR containing the GluN2B subunit triggers excitotoxicity during ischemic stroke and subsequent neuronal apoptosis, whereas activation of NMDAR containing the GluN2A subunit exerts a neuroprotective effect. Therefore, analyzing the molecular mechanism of NMDA receptor-mediated excitotoxicity in stroke is of great significance for the development of new neuroprotective agents targeting different NMDAR subtypes.

Fig. 1. NMDARs play a key role in excitotoxicity induced by ischemic stroke.Fig. 1. Distinct subpopulations of the NMDAR mediate neuronal death and survival. (Lai et al., 2014)

Our Services

As a leading CRO in the stroke field, Ace Therapeutics delves into the complex molecular pathways underlying excitotoxicity, with a special focus on the molecular mechanisms of NMDAR-mediated excitotoxicity in stroke. We aim to help our clients identify the different intracellular pathways that link NMDAR activation to neuronal death, enabling them to develop new therapies that target specific cell death signaling pathways without affecting all signaling pathways downstream of the receptor.

Analyzing the mechanisms of glutamate-mediated NMDAR activation in stroke

Based on cellular and molecular biology platforms, our dedicated team of experts analyzes the mechanisms by which glutamate-mediated NMDAR activation in stroke transmits different functional outputs at the microscopic neuronal level and macroscopic behavioral level through detailed experiments and advanced technologies.

Elucidating the NMDAR downstream signaling pathways

We provide comprehensive proteomics and transcriptomics services to analyze the downstream cell survival and death signaling pathways mediated by NR2A and NR2B. More NMDAR downstream signaling pathways analysis services are under development and can be customized according to customer specifics.

NMDAR-mediated downstream cellular survival signaling pathways (NR2A targets) CREB-BDNF, ERK, PI3K/Akt, and Kidins220-ARMS signaling pathways
NMDAR-mediated downstream cellular death signaling pathways (NR2B targets) DAPK1, PSD95-nNOS, autophagy-inflammation related signaling (e.g. mTORC1, AMPK, p38MAPK), calpain, and SUR1-TRPM4 signaling pathway

Our Approaches

Ace Therapeutics utilizes a multidisciplinary approach that integrates advanced techniques in molecular biology, neurophysiology, and bioinformatics to unravel the molecular mechanisms of NMDAR-mediated excitotoxicity in stroke.

Excitotoxicity In Vitro Assay

Using primary neuronal cultures and organotypic brain slices, we reproduce ischemic conditions in a controlled experimental setting to elucidate the molecular events behind NMDAR-mediated excitotoxicity. Through pharmacological manipulations and genetic interventions, we dissect the contribution of specific signaling pathways to neuronal damage.

In Vivo Assays

Ace Therapeutics conducts preclinical studies using animal models of ischemic stroke to validate our findings in a physiological context. We use behavioral assessments, histological analyses, and in vivo imaging techniques to assess the efficacy of novel therapeutic interventions targeting NMDAR-mediated excitotoxicity.

Ace Therapeutics provides comprehensive molecular mechanism analysis services to elucidate the role of NMDAR-mediated excitotoxicity in stroke pathogenesis. Through advanced methodologies and partnerships, we help clients develop stroke drugs that selectively inhibit NMDAR overactivation while preserving or restoring its normal activity. If you are interested in our services, please do not hesitate to contact us!

  1. Lai, T. W., et al. (2014). Excitotoxicity and stroke: identifying novel targets for neuroprotection. Progress in neurobiology, 115, 157-188.
All of our services are intended for preclinical research use only and cannot be used to diagnose, treat or manage patients.
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