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Updated: Feb 2, 2026

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Enlarged Optic Nerve Axons and Reduced Visual Function in Mice with Defective Microfibrils.

Hang-Jing Wu1, Ralph J Hazlewood1, John Kuchtey1

  • 1Vanderbilt Eye Institute, Vanderbilt University Medical Center, Nashville, TN 37232-8808.

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PubMed
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Microfibril defects, caused by fibrilin-1 gene mutations, can lead to early-stage glaucoma phenotypes in mice, including retinal ganglion cell (RGC) dysfunction and optic nerve changes, independent of intraocular pressure.

Keywords:
biomechanical propertyglaucomamicrofibriloptic nerveretinal ganglion cellsvisual function

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Area of Science:

  • Ophthalmology
  • Neuroscience
  • Genetics

Background:

  • Glaucoma is a leading cause of irreversible vision loss, characterized by retinal ganglion cell (RGC) degeneration.
  • Elevated intraocular pressure (IOP) is a major risk factor, but glaucoma can occur with normal IOP.
  • Mutations in microfibril-associated genes are implicated in glaucoma, suggesting a role for microfibril defects.

Purpose of the Study:

  • To investigate the role of microfibril abnormalities in glaucoma pathogenesis.
  • To examine IOP, RGC degeneration, and optic nerve structure in mice with heterozygous fibrilin-1 gene (Fbn1+/+) mutations.

Main Methods:

  • Utilized heterozygous Fbn1+/+ mice with abnormal microfibrils.
  • Assessed intraocular pressure (IOP).
  • Evaluated functional and structural correlates of RGC degeneration using electroretinogram (ERG) and optic nerve axon density/diameter analysis.

Main Results:

  • Fbn1+/+ mice showed functional deficits consistent with glaucoma at advanced age, including reduced RGC responses in ERG.
  • Retinal RGC density was unaffected, but optic nerve RGC axon density was reduced.
  • Optic nerves were expanded in Fbn1+/+ mice, with enlarged axons, correlating with optic nerve area.
  • Thinning of the pia mater was observed, suggesting a mechanism for optic nerve expansion and axon caliber determination.

Conclusions:

  • Microfibril abnormalities can induce phenotypes observed in early-stage glaucomatous neurodegeneration.
  • These findings suggest a potential biomechanical contribution of microfibrils to glaucoma pathogenesis.
  • The study highlights microfibril defects as a potential factor in glaucoma development, even with normal IOP.