Neuroinflammation Glaucoma
Neuroinflammation Glaucoma - Related Videos
02:28
Inducing Neuroinflammation in Zebrafish Larvae with a Lipopolysaccharide Injection
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2025
The video demonstrates the microinjection of lipopolysaccharides (LPS) into the brains of zebrafish larvae to induce neuroinflammation. The larvae are positioned on an agarose-lined dish, the needle is inserted into the brain ventricles, and the LPS is injected. The injected LPS triggers an immune response that leads to neuroinflammation.
03:07
Bioluminescence Imaging of Neuroinflammation in a Transgenic Mouse
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2025
Source: Breid, S., et. al. Bioluminescence Imaging of Neuroinflammation in Transgenic Mice After Peripheral Inoculation of Alpha-Synuclein Fibrils. J. Vis. Exp. (2017)This video demonstrates the bioluminescence imaging of neuroinflammation in transgenic mice, showcasing luciferase-luciferin reactions in activated astrocytes. The protocol enables non-invasive quantification of astrocytic activation, aiding studies on CNS inflammation and therapeutic efficacy.
05:05
Ultrasound Cyclo Plasty in Eyes with Glaucoma
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Cited by 17 •
2018
Glaucoma is a chronic disease with progressive degeneration of optic nerve fibers resulting in decreased visual field. Elevated intraocular pressure is considered the most important and the only treatable risk factor. This manuscript describes a simple, surgeon-friendly, non-incisional technique, named Ultrasound Cyclo Plasty, for reducing intraocular pressure in glaucoma patients.
02:12
Induction of Neuroinflammation in Mice via Injection of Alpha-Synuclein Fibrils
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2025
This video demonstrates the injection of alpha-synuclein fibrils into a mouse to induce neuroinflammation. The fibrils are injected intraperitoneally into a transgenic mouse expressing mutated alpha-synuclein proteins. Upon reaching the central nervous system, the fibrils enter neurons and induce aggregation of the mutated proteins. The aggregates spread to neighboring neurons, microglia, and astrocytes. Recognition of the aggregates triggers microglia to induce neuroinflammation, damaging the...
02:00
Generating Virus-Induced Neuroinflammation in a Mouse Model
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2025
This video demonstrates the generation of neuroinflammation in a mouse model. An anesthetized mouse with micro-wounds is taken, and an inoculum of pseudorabies virus (PRV) is applied to the wounds. The virus infects the peripheral nerves, spreads to the dorsal root ganglia (DRG), and further infects the spinal cord and brain. Infection of neurons in the nervous system leads to an immune response that induces neuronal damage, leading to neuroinflammation.
FAQs
Tissue stress, elevated intraocular pressure, and neural injury can activate microglia and astrocytes in the retina and optic nerve. Once activated, these cells release cytokines and other inflammatory mediators that modify the local neural environment. Their activity is therefore relevant to retinal ganglion cell survival and may help explain how inflammatory signaling contributes to progressive visual damage.
Pressure control addresses an important source of tissue stress, but it may not eliminate inflammatory changes that have already developed in neural tissues. Activated microglia and astrocytes can continue releasing cytokines and other mediators that affect neuronal survival, axonal transport, and the optic nerve environment. This provides a biological rationale for studying inflammation alongside pressure-related mechanisms.
These mediators can alter several processes linked to neural function, including retinal ganglion cell survival, movement of materials along axons, and conditions within the optic nerve. Their effects are important because damage may arise not only from the initiating stress but also from changes in the surrounding neural environment. Measuring these pathways can help connect immune activity with vision loss.
Each of these conditions can provide a signal associated with activation of microglia and astrocytes in the retina and optic nerve. The resulting cellular response may change inflammatory mediator release and the local support environment for neurons and axons. Studying these relationships helps biology researchers examine how physical or neural stress becomes linked to progressive retinal ganglion cell damage.
Research can focus on microglial and astrocyte activation, cytokines and other inflammatory mediators, retinal ganglion cell survival, axonal transport, and the optic nerve environment. Together, these features provide complementary information about immune activity and neural injury. Such measurements can help identify biomarkers associated with disease progression and clarify which processes might be suitable for therapeutic investigation.
Understanding these mechanisms can guide investigation of treatments designed to modulate inflammation, protect neural tissue, or preserve visual function. The goal is not limited to lowering intraocular pressure; it also includes addressing inflammatory effects on neurons, axons, and the optic nerve environment. Biomarker research may further help evaluate inflammatory activity and treatment-related changes during disease study.