|Year : 2015 | Volume
| Issue : 4 | Page : 503-504
Ahmad A Aref MD , Sachin Jain MD
Department of Ophthalmology and Visual Sciences, Illinois Eye and Ear Infirmary, University of Illinois at Chicago College of Medicine, Chicago, IL, USA
|Date of Submission||30-Oct-2015|
|Date of Acceptance||30-Dec-2015|
|Date of Web Publication||18-Feb-2016|
Ahmad A Aref
Department of Ophthalmology and Visual Sciences, Illinois Eye and Ear Infirmary, University of Illinois College of Medicine, 1855 W. Taylor Street, Unit 3.171 Chicago, IL 60612
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Aref AA, Jain S. Author's reply. J Ophthalmic Vis Res 2015;10:503-4
We appreciate Dr. Wostyn, et al's interest in our manuscript titled, “Senile Dementia and Glaucoma: Evidence for a Common Link”. Dr. Wostynet al's work in this area is indeed intriguing. Dr. Wostynet al's hypothesis states that deficient exchange between cerebrospinal fluid and brain interstitial fluid compartments along the optic nerve may allow the accumulation of neurotoxins, including amyloid-β, and subsequently predispose to glaucomatous optic neuropathy. Specifically, this deficiency in waste exchange could occur within a network of diseased paravenous drainage pathways. The glymphatic pathway, as described by Iliffet al, may become dysfunctional due to genetic insult to the Aqp4 gene, which regulates generation of the water channel aquaporin-4 in astrocytes. Animals with deletion of the Aqp4 gene exhibit decreased clearance of amyloid-β via the glymphatic pathway.
Given the potential link between Alzheimer's disease and glaucomatous optic neuropathy, we agree that the aforementioned findings may have important implications regarding the pathophysiology and possible therapy for certain forms of glaucomatous optic neuropathy. It would be interesting to investigate the effects of suppression of the Aqp4 gene on optic nerve health. Possible subsequent glaucomatous optic neuropathy, presumably due to accumulation of amyloid-β via a dysfunctional glymphatic pathway, would strongly support the link between Alzheimer's disease and “normal tension” types of glaucoma. Furthermore, this would offer a potential therapeutic target for both diseases.
Financial Support and Sponsorship
The authors are supported by NIH Core Grant EY001792 and an Unrestricted Grant from Research to Prevent Blindness.
Conflicts of Interest
There are no conflicts of interest.
| References|| |
Jain S, Aref AA. Senile dementia and glaucoma: Evidence for a common link. J Ophthalmic Vis Res
Wostyn P, Van Dam D, Audenaert K, Killer HE, De Deyn PP, De Groot V, et al. A new glaucoma hypothesis: A role of glymphatic system dysfunction. Fluids Barriers CNS
Iliff JJ, Wang M, Liao Y, Plogg BA, Peng W, Gundersen GA, et al. A paravascular pathway facilitates CSF flow through the brain parenchyma and the clearance of interstitial solutes, including amyloid β. Sci Transl Med