At Ace Therapeutics, we are dedicated to providing highly translational models with robust construct, face, and predictive validity that are sensitive to the neurodegenerative changes observed in glaucoma. Our custom excitatory amino acid-induced glaucoma models provide a powerful means to investigate the basic neuropathology underlying this complex disease, offering researchers a robust platform to study the neurodegenerative mechanisms and identify novel therapeutic targets.
Excitatory Amino Acids and Glaucoma
Excitatory amino acids (EAAs), particularly glutamate and aspartate, are central to the neurodegenerative cascades observed in glaucoma. Excessive glutamate release in the retina activates N-methyl-D-aspartate (NMDA) receptors, triggering a cascade of pathological events, including Ca²⁺ overload, mitochondrial dysfunction, and oxidative stress. These events collectively drive retinal ganglion cell (RGC) apoptosis—a hallmark of glaucoma progression. Chronic EAA excitotoxicity mirrors human disease progression, making these EAA-induced glaucoma models critical for studying therapeutics such as NMDA receptor antagonists and neuroprotective agents.
Fig. 1 NMDA-induced glaucoma mouse model is successfully established. (Niu Y L, et al., 2024)
Explore Our Excitatory Amino Acid-Induced Glaucoma Models
Our excitatory amino acid-induced glaucoma models are widely used to study the neurodegenerative mechanisms due to their ability to recapitulate key features of human glaucoma.
NMDA-Induced Glaucoma Models
We utilize intravitreal injection of NMDA to selectively activate retinal NMDA receptors, inducing Ca²⁺ overload and RGC apoptosis. This approach recapitulates synaptic glutamate excitotoxicity observed in early-stage glaucoma. Our NMDA-induced glaucoma models are ideal for testing NMDA receptor antagonists and neuroprotective agents that target calcium dysregulation.
Glutamate-Induced Glaucoma Models
Our team employs intravitreal injection of glutamate to induce prolonged activation of retinal glutamate receptors, leading to Ca²⁺ overload, oxidative stress, and subsequent RGC apoptosis. This method recapitulates the chronic excitotoxicity and neurodegenerative changes characteristic of glaucoma progression. Our glutamate-induced glaucoma models are well suited for studying the long-term effects of glutamate excitotoxicity and evaluating therapeutic strategies targeting oxidative stress and neuroprotection.
Characteristics and Advantages of Our Excitatory Amino Acid-Induced Glaucoma Models
- High pathophysiological fidelity
Our models reproduce key features of glaucoma, including RGC loss, optic nerve degeneration, and functional vision deficits. - Customizability
Designed to meet specific research needs, our models offer the flexibility to be customized in dosing, timing, and the use of different animal species. - Robust validation
Our models undergo rigorous validation through histological, molecular, and functional assessments to ensure reliability and consistency.
Applications of Excitatory Amino Acid-Induced Glaucoma Models
Our excitatory amino acid-induced glaucoma models can be applied in multiple areas, and we provide related services to support these applications.
- Glaucoma pathogenesis studies
Elucidate EAA-mediated excitotoxic mechanisms in retinal ganglion cell degeneration. - Drug screening
High-throughput screening of potential therapeutic compounds for their ability to mitigate excitotoxic damage and promote neuroprotection. - Efficacy evaluation
Assess neuroprotective compounds by functional (ERG, visual acuity) and histological (RGC survival) endpoints. - Biomarker discovery
Identify and validate glaucoma biomarkers through proteomic profiling.
Ace Therapeutics is your trusted preclinical contract service provider for basic research and drug development, offering custom models and tailored solutions. Our excitatory amino acid-induced glaucoma models recapitulate optic nerve atrophy and visual field deficits, supporting preclinical evaluation of candidate drugs aimed at halting RGC loss. Ready to discuss your programs? Contact us now!
Reference
- Niu Y L, et al. Relationship Between Changes in the Expression Levels of miR-134 and E2F6 in Mediating Control of Apoptosis in NMDA-Induced Glaucomatous Mice. J Invest Surg, 2024, 37(1):2389379.