title: A new glaucoma hypothesis: a role of glymphatic system dysfunction.
abstract: In a recent review article titled "A new look at cerebrospinal fluid circulation", Brinker et al. comprehensively described novel insights from molecular and cellular biology as well as neuroimaging research, which indicate that cerebrospinal fluid (CSF) physiology is much more complex than previously believed. The glymphatic system is a recently defined brain-wide paravascular pathway for CSF and interstitial fluid exchange that facilitates efficient clearance of interstitial solutes, including amyloid-β, from the brain. Although further studies are needed to substantiate the functional significance of the glymphatic concept, one implication is that glymphatic pathway dysfunction may contribute to the deficient amyloid-β clearance in Alzheimer's disease. In this paper, we review several lines of evidence suggesting that the glymphatic system may also have potential clinical relevance for the understanding of glaucoma. As a clinically acceptable MRI-based approach to evaluate glymphatic pathway function in humans has recently been developed, a unique opportunity now exists to investigate whether suppression of the glymphatic system contributes to the development of glaucoma. The observation of a dysfunctional glymphatic system in patients with glaucoma would provide support for the hypothesis recently proposed by our group that CSF circulatory dysfunction may play a contributory role in the pathogenesis of glaucomatous damage. This would suggest a new hypothesis for glaucoma, which, just like Alzheimer's disease, might be considered then as an imbalance between production and clearance of neurotoxins, including amyloid-β.
authors.affiliation: Department of Psychiatry, PC Sint-Amandus, Reigerlostraat 10, 8730, Beernem, Belgium. wostyn.peter@skynet.be.
authors.forename: Peter
authors.initials: P
authors.lastname: Wostyn
authors.affiliation: Department of Biomedical Sciences, Laboratory of Neurochemistry and Behavior, Institute Born-Bunge, University of Antwerp, Universiteitsplein 1, 2610, Antwerp, Belgium. debby.vandam@uantwerpen.be.
authors.forename: Debby
authors.initials: D
authors.lastname: Van Dam
authors.affiliation: Department of Psychiatry, Ghent University Hospital, De Pintelaan 185, 9000, Ghent, Belgium. kaudenae@me.com.
authors.forename: Kurt
authors.initials: K
authors.lastname: Audenaert
authors.affiliation: Department of Ophthalmology, Kantonsspital Aarau, Buchserstrasse, Aarau, 5001, Switzerland. Hanspeter.Killer@ksa.ch.
authors.forename: Hanspeter Esriel
authors.initials: HE
authors.lastname: Killer
authors.affiliation: Department of Biomedical Sciences, Laboratory of Neurochemistry and Behavior, Institute Born-Bunge, University of Antwerp, Universiteitsplein 1, 2610, Antwerp, Belgium. dedeyn@skynet.be.|Department of Neurology and Memory Clinic, Middelheim General Hospital (ZNA), Lindendreef 1, 2020, Antwerp, Belgium. dedeyn@skynet.be.|Department of Neurology and Alzheimer Research Center, University of Groningen and University Medical Center Groningen, Hanzeplein 1, 9700 RB, Groningen, The Netherlands. dedeyn@skynet.be.
authors.forename: Peter Paul
authors.initials: PP
authors.lastname: De Deyn
authors.affiliation: Department of Ophthalmology, Antwerp University Hospital, Wilrijkstraat 10, 2650, Antwerp, Belgium. Veva.DeGroot@uza.be.
authors.forename: Veva
authors.initials: V
authors.lastname: De Groot
mesh_terms: D016229:Amyloid beta-Peptides / Q000378:metabolism; D001921:Brain / Q000098:blood supply*; D002555:Cerebrospinal Fluid / Q000378:metabolism*; D045604:Extracellular Fluid / Q000378:metabolism; D005901:Glaucoma / Q000134:cerebrospinal fluid* / Q000209:etiology / Q000503:physiopathology*; D006801:Humans; D008297:Male; D009900:Optic Nerve / Q000503:physiopathology; D016875:tau Proteins / Q000378:metabolism
chemical_list: D016229:Amyloid beta-Peptides; D016875:tau Proteins