Ace Therapeutics provides comprehensive services centered around TNF-α-induced glaucoma models. By recapitulating TNF-α-driven neurodegeneration, our animal models enable robust evaluation of therapeutic candidates.
TNF-α in Glaucoma Pathogenesis
Glaucoma is a leading cause of irreversible vision loss, characterized by progressive damage to retinal ganglion cells (RGCs) and the optic nerve. Tumor necrosis factor-alpha (TNF-α) is a key cytokine involved in both neuroprotective and neurodegenerative processes. Elevated levels of TNF-α have been implicated in the pathogenesis of glaucoma. TNF-α drives neuroinflammation and RGC apoptosis, contributing to optic nerve damage and RGC loss. TNF-α-induced glaucoma models mimic these inflammatory pathways, offering a valuable tool for studying disease mechanisms and evaluating neuroprotective interventions.
Fig. 1 Role of TNF-α in retinal ganglion cell apoptosis induced by elevated intraocular pressure and retinal ischemia. (Agarwal R and Agarwal P, 2012)
Explore TNF-α-Induced Glaucoma Model Customization Solutions
Ace Therapeutics provides tailored TNF-α-induced glaucoma models designed to replicate the neuroinflammatory processes observed in glaucoma.
- Species selection
We provide TNF-α-induced glaucoma models in rodents (e.g., mice and rats), rabbits, and non-human primates, with customization available for other species based on your specific research needs. - Induction methods
Our TNF-α-induced glaucoma models are typically established by intravitreal injection to effectively induce TNF-α-mediated neuroinflammation. - Dose optimization
Our dose optimization services for TNF-α administration in glaucoma models ensure precise concentration and exposure duration, enabling consistent and reproducible neuroinflammatory responses for preclinical studies. Our team works closely with clients to tailor dosing protocols based on specific research goals and species requirements.
Available Support Services for Our TNF-α-Induced Glaucoma Models
We offer comprehensive support services tailored to provide in-depth insights into disease mechanisms and therapeutic efficacy for our clients.
Protein Level Analysis of TNF-α
- TNF-α level measurement
Quantitatively measure TNF-α levels in ocular samples (e.g., aqueous humor, vitreous, serum) to validate the successful establishment of the models and assess the efficacy of candidate drugs. - Analysis of TNF-α protein expression
Analyze TNF-α protein expression and downstream signaling (e.g., NF-κB activation) in retinal or optic nerve tissues to elucidate molecular mechanisms.
Assessment of Neurodegeneration and Neural Repair
- Axonal damage markers
Detect abnormal axonal accumulation in optic nerve sections to evaluate TNF-α-mediated neurodegeneration. - Neurotrophic factors
Measure levels of neurotrophic factors using qPCR or ELISA to assess neuroregenerative potential elicited by therapeutics.
Functional Assessments
- Optical coherence tomography (OCT)
Quantify retinal layer thickness (e.g., ganglion cell layer) and detect structural changes in animal models. - Fundus photography
Monitor vascular abnormalities, optic disc cupping, and retinal nerve fiber layer defects (RNFLDs). - Pattern electroretinogram (PERG)
Measure RGC electrical activity to assess functional integrity.
Ace Therapeutics is comprised of leading experts in glaucoma research. Our TNF-α-induced glaucoma models undergo rigorous validation and quality control to ensure model reliability and reproducibility. Contact us to learn more about our comprehensive technical and scientific support throughout your project!
Reference
- Agarwal R, Agarwal P. Glaucomatous neurodegeneration: An eye on tumor necrosis factor-alpha. Indian J Ophthalmol, 2012, 60(4):255-261.