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Related Concept Videos

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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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.
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DBA/2J mouse model for experimental glaucoma: pitfalls and problems.

Anita J Turner1, Roshana Vander Wall1, Vivek Gupta1

  • 1Faculty of Medicine and Health Sciences, Macquarie University, Sydney, New South Wales, Australia.

Clinical & Experimental Ophthalmology
|May 19, 2017
PubMed
Summary
This summary is machine-generated.

The DBA/2J mouse model for glaucoma presents significant challenges for research due to unreliable intraocular pressure measurements and high dropout rates. These issues complicate drug studies and assessing disease progression in experimental glaucoma.

Keywords:
DBA/2Jglaucomamouse model

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Area of Science:

  • Ophthalmology
  • Neuroscience
  • Genetics

Background:

  • The DBA/2J mouse is a model for congenital experimental glaucoma, exhibiting anterior segment anomalies, synechiae, and pigment dispersion.
  • These anomalies lead to elevated intraocular pressure and glaucomatous damage, but practical limitations exist for longitudinal studies.

Purpose of the Study:

  • To evaluate the utility of the DBA/2J mouse model in longitudinal glaucoma studies.
  • To identify challenges and confounding factors in using this model for pharmaceutical trials.

Main Methods:

  • Followed 118 mice (37 controls) from 12-48 weeks.
  • Weekly intraocular pressure (IOP) measurements, with electrophysiology and optical coherence tomography (OCT) every 6 weeks.
  • Invasive IOP measurements performed on a subset prior to euthanasia.

Main Results:

  • Corneal calcification in most mice rendered non-invasive IOP measurements unreliable.
  • Invasive IOP did not correlate with non-invasive measures.
  • Glaucomatous damage (vision loss, retinal thinning) observed in some mice without elevated IOP.
  • Poor pupil dilation impacted imaging and electrophysiology; 22% dropout rate due to systemic complications.

Conclusions:

  • The DBA/2J model exhibits significant variability and pathological changes that hinder disease progression assessment.
  • Challenges include unreliable IOP measurement, difficulties with in vivo imaging and electrophysiology, and high dropout rates.
  • Potential underlying neurodegenerative processes independent of IOP require consideration.