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Glymphatic stasis at the site of the lamina cribrosa as a potential mechanism underlying open-angle glaucoma.

  • Wostyn P Department of Psychiatry, PC Sint-Amandus, Beernem, Belgium.
  • Killer HE Department of Ophthalmology, Kantonsspital Aarau, Aarau, Switzerland.
  • De Deyn PP Laboratory of Neurochemistry and Behavior. Institute Born-Bunge, Department of Biomedical Sciences, University of Antwerp, Antwerp, Belgium.
  • 2017-01-28
Published in:
  • Clinical & experimental ophthalmology. - 2017
glaucoma
intracranial pressure
intraocular pressure
lamina cribrosa
trans-lamina cribrosa pressure difference
Animals
Cerebrospinal Fluid Pressure
Glaucoma, Open-Angle
Humans
Intraocular Pressure
Optic Disk
Retinal Ganglion Cells
Tonometry, Ocular
English The underlying pathophysiology of primary open-angle glaucoma remains unclear, but the lamina cribrosa seems to be the primary site of injury, and raised intraocular pressure is a major risk factor. In recent years, a decreased intracranial pressure, leading to an abnormally high trans-lamina cribrosa pressure difference, has gained interest as a new risk factor for glaucoma. New research now lends support to the hypothesis that a paravascular transport system is present in the eye analogous to the recently discovered 'glymphatic system' in the brain, which is a functional waste clearance pathway that promotes elimination of interstitial solutes, including β-amyloid, from the brain along paravascular channels. Given that β-amyloid has been reported to increase by chronic elevation of intraocular pressure in glaucomatous animal models and to cause retinal ganglion cell death, the discovery of a paravascular clearance system in the eye may provide powerful new insights into the pathophysiology of primary open-angle glaucoma. In this review, we provide a new conceptual framework for understanding the pathogenesis of primary open-angle glaucoma, present supporting preliminary data from our own post-mortem study and hypothesize that the disease may result from restriction of normal glymphatic flow at the level of the lamina cribrosa owing to a low intracranial pressure and/or a high trans-lamina cribrosa pressure gradient. If confirmed, this viewpoint could offer new perspectives for the development of novel diagnostic and therapeutic strategies for this devastating disorder.
Language
  • English
Open access status
hybrid
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https://sonar.ch/global/documents/281034
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