Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Glaucoma: Overview01:25

Glaucoma: Overview

Glaucoma is an eye condition characterized by increased intraocular pressure that damages the retina and optic nerve, leading to irreversible blindness if left untreated. The human eye has various components, including the cornea, iris, pupil, lens, and optic nerve. Aqueous humor is secreted by the epithelium of the ciliary body in the posterior chamber and flows through the trabecular meshwork and canal of Schlemm, maintaining normal intraocular pressure. The trabecular meshwork and the canal...
Open Angle Glaucoma: Treatment01:27

Open Angle Glaucoma: Treatment

In open-angle glaucoma, the iridocorneal angle remains open, but the trabecular meshwork becomes stiff, slowing down the outflow of aqueous humor. This causes a buildup of aqueous humor in the anterior chamber, leading to a sudden increase in intraocular pressure. The treatment for open-angle glaucoma focuses on reducing the elevated intraocular pressure by either decreasing the secretion of aqueous humor or increasing its outflow.
Drugs such as carbonic anhydrase inhibitors, α2- and...
Angle Closure Glaucoma: Treatment01:28

Angle Closure Glaucoma: Treatment

Angle-closure glaucoma, or closed-angle glaucoma, is an eye condition where the iris bulges out and blocks the iridocorneal angle, resulting in a buildup of aqueous humor and increased intraocular pressure. Immediate medical attention is necessary due to the sudden onset of symptoms. The treatment for angle-closure glaucoma includes short-term and long-term approaches. Short-term treatment involves using eye drops like pilocarpine to lower intraocular pressure by increasing aqueous humor...
Diabetic Retinopathy01:27

Diabetic Retinopathy

DefinitionDiabetic retinopathy is a microvascular complication of diabetes affecting the retinal blood vessels.Risk FactorsDiabetic retinopathy is present in almost all individuals with type 1 diabetes and more than 60% of those with type 2 diabetes after two decades of disease.The risk increases with poor glycemic control, hypertension, dyslipidemia, smoking, pregnancy, and puberty.Although cataracts and glaucoma are also more frequent in people with diabetes, retinopathy remains the leading...
Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
Increased Intracranial Pressure ll: Pathophysiology01:29

Increased Intracranial Pressure ll: Pathophysiology

Increased intracranial pressure (ICP) refers to a potentially life-threatening rise in pressure inside the skull. This usually happens when there is a major change in the volume of brain tissue, blood, or cerebrospinal fluid (CSF) — the three components inside the skull. According to the Monro-Kellie doctrine, if the volume of one component increases, the volumes of the other components must decrease to maintain normal pressure. If this does not happen, ICP rises.The process often begins with...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Dynamics of the association between visual and auditory functional changes in glaucoma. Preliminary results.

Romanian journal of ophthalmology·2023
Same author

Glaucoma - a neurodegenerative disease with cerebral neuroconnectivity elements.

Romanian journal of ophthalmology·2022
Same author

IMPORTANCE OF DEMOGRAPHIC RISK FACTORS FOR PRIMARY ANGLE CLOSURE.

Romanian journal of ophthalmology·2016
Same author

[Glaucoma County Center].

Oftalmologia (Bucharest, Romania : 1990)·2011
Same author

[Receptors involved in the mechanism of action of topical prostaglandines].

Oftalmologia (Bucharest, Romania : 1990)·2009

Related Experiment Video

Updated: Jul 20, 2026

Glaucoma-inducing Procedure in an In Vivo Rat Model and Whole-mount Retina Preparation
08:30

Glaucoma-inducing Procedure in an In Vivo Rat Model and Whole-mount Retina Preparation

Published on: March 12, 2016

[Etiopathogenic mechanisms in glaucoma].

Alina Mihaela Neacşu1

  • 1Spital Judeţean de Urgenţă, Brăila.

Oftalmologia (Bucharest, Romania : 1990)
|August 25, 2006
PubMed
Summary

Glaucoma is a complex eye disease. Understanding the mechanisms of ganglion cell destruction is key to developing new therapies that protect vision.

Area of Science:

  • Ophthalmology
  • Neuroscience

Background:

  • Glaucoma is a leading cause of irreversible blindness worldwide.
  • It is characterized by progressive damage to retinal ganglion cells (RGCs).
  • The multifactorial nature of glaucoma necessitates a comprehensive understanding of RGCs destruction.

Purpose of the Study:

  • To identify the key mechanisms underlying retinal ganglion cells (RGCs) destruction in glaucoma.
  • To explore potential therapeutic targets for halting RGCs death.
  • To support the natural defense mechanisms of RGCs.

Main Methods:

  • This study involves a review of current literature on glaucoma pathogenesis.
  • Analysis of molecular and cellular pathways implicated in RGCs apoptosis.
  • Investigation of neuroprotective strategies.

More Related Videos

Full-Circle Cauterization of Limbal Vascular Plexus for Surgically Induced Glaucoma in Rodents
10:10

Full-Circle Cauterization of Limbal Vascular Plexus for Surgically Induced Glaucoma in Rodents

Published on: February 15, 2022

Translaminar Autonomous System Model for the Modulation of Intraocular and Intracranial Pressure in Human Donor Posterior Segments
08:55

Translaminar Autonomous System Model for the Modulation of Intraocular and Intracranial Pressure in Human Donor Posterior Segments

Published on: April 24, 2020

Related Experiment Videos

Last Updated: Jul 20, 2026

Glaucoma-inducing Procedure in an In Vivo Rat Model and Whole-mount Retina Preparation
08:30

Glaucoma-inducing Procedure in an In Vivo Rat Model and Whole-mount Retina Preparation

Published on: March 12, 2016

Full-Circle Cauterization of Limbal Vascular Plexus for Surgically Induced Glaucoma in Rodents
10:10

Full-Circle Cauterization of Limbal Vascular Plexus for Surgically Induced Glaucoma in Rodents

Published on: February 15, 2022

Translaminar Autonomous System Model for the Modulation of Intraocular and Intracranial Pressure in Human Donor Posterior Segments
08:55

Translaminar Autonomous System Model for the Modulation of Intraocular and Intracranial Pressure in Human Donor Posterior Segments

Published on: April 24, 2020

Main Results:

  • Multiple pathways contribute to RGCs degeneration, including oxidative stress, excitotoxicity, and inflammation.
  • Identifying these pathways offers opportunities for targeted interventions.
  • Understanding natural defense mechanisms can inform therapeutic development.

Conclusions:

  • A thorough understanding of glaucoma's multifactorial mechanisms is crucial for developing effective treatments.
  • Targeting RGCs destruction pathways holds promise for preventing vision loss.
  • Future research should focus on translating these findings into clinical applications.