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Related Concept Videos

Open Angle Glaucoma: Treatment01:27

Open Angle Glaucoma: Treatment

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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...
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Angle Closure Glaucoma: Treatment01:28

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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...
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Glaucoma: Overview01:25

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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...
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Related Experiment Video

Updated: Jan 16, 2026

Assessing Early Stage Open-Angle Glaucoma in Patients by Isolated-Check Visual Evoked Potential
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Profiling lipidomic variations in primary open-angle and angle-closure glaucoma patients.

Lakshminarayanan Gowtham1, Nabanita Halder1, Dewang Angmo2

  • 1Department of Ocular Pharmacology and Pharmacy Division, Dr. Rajendra Prasad Centre for Ophthalmic Sciences, All India Institute of Medical Sciences, New Delhi, India.

Experimental Eye Research
|September 25, 2025
PubMed
Summary

Glaucoma patients show altered lipid profiles in aqueous humor and plasma, with specific changes in sphingomyelins and ceramides in angle-closure glaucoma. These lipid alterations may serve as biomarkers for retinal degeneration and apoptosis in glaucoma.

Keywords:
Aqueous humorLipidomicsMass spectrometryPlasmaPrimary open angle and angle closure glaucoma

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Sample Preparation for Mass-spectrometry-based Proteomics Analysis of Ocular Microvessels
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Area of Science:

  • Ophthalmology
  • Lipidomics
  • Biochemistry

Background:

  • Glaucoma causes irreversible vision loss due to retinal ganglion cell death.
  • Investigating lipid profiles in ocular fluids and plasma may reveal novel biomarkers and signaling pathways.
  • Systemic lipid alterations can be compared with ocular changes for accessible biomarker discovery.

Purpose of the Study:

  • To investigate and compare lipidomic profiles in aqueous humor and plasma of primary open-angle glaucoma (POAG), angle-closure glaucoma (PACG), and cataract control groups.
  • To identify potential lipid biomarkers associated with glaucoma pathogenesis.
  • To explore systemic versus ocular lipid alterations in glaucoma patients.

Main Methods:

  • Collected aqueous humor and plasma samples from 20 POAG patients, 20 PACG patients, and 20 cataract controls.
  • Analyzed lipids using high-resolution mass spectrometry (HRMS) and quantified species with LipidSearch™.
  • Performed statistical analyses using MetaboAnalyst 5.0 with defined significance criteria (log2 FC, p-value, VIP score).

Main Results:

  • Routine serum lipid profiles showed no significant differences between glaucoma patients and controls.
  • Aqueous humor revealed elevated phosphatidylcholines and lysophosphatidylcholines in both glaucoma groups.
  • PACG patients specifically showed elevated sphingomyelins and ceramides in aqueous humor; plasma showed decreased diglycerides, triglycerides, and cholesterol esters in both glaucoma groups.

Conclusions:

  • Sphingomyelin and ceramide alterations in PACG aqueous humor suggest disrupted mechanosignaling.
  • Elevated phosphatidylcholines, lysophosphatidylcholines, and altered glycerides in aqueous humor are linked to retinal degeneration and apoptosis in glaucoma.
  • Lipidomic analysis of aqueous humor and plasma offers insights into glaucoma pathophysiology and potential biomarker identification.