Age- and glaucoma-induced changes to the ocular glymphatic system

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The ocular glymphatic system supports bidirectional fluid transport along the optic nerve, thereby removes metabolic wastes including amyloid-β. To better understand this biological process, we examined the distributions of intravitreally and intracisternally infused tracers in full-length optic nerves from different age groups of mice. Aging was linked to globally impaired ocular glymphatic fluid transport, similar to what has seen previously in the brain. Aging also reduced the pupillary responsiveness to light stimulation and abolished light-induced facilitation in anterograde ocular glymphatic flow. In contrast to normal aging, in the DBA/2 J model of glaucoma, we found a pathological increase of glymphatic fluid transport to the anterior optic nerve that was associated with dilation of the perivascular spaces. Thus, aging and glaucoma have fundamentally different effects on ocular glymphatic fluid transport. Manipulation of glymphatic fluid transport might therefore present a new target for the treatment of glaucoma.
OriginalsprogEngelsk
Artikelnummer106322
TidsskriftNeurobiology of Disease
Vol/bind188
Antal sider9
ISSN0969-9961
DOI
StatusUdgivet - 2023

Bibliografisk note

Funding Information:
This project has received funding from the European Research Council (ERC) under the European Union's Horizon 2020 research and innovation programme (grant agreement no. 742112 ), the Novo Nordisk and the Lundbeck Foundations , Dr. Miriam and Sheldon G. Adelson Medical Research Foundation , the NIH/NINDS/NIA ( R01NS100366 and RF1AG057575 ), the Research to Prevent Blindness Foundation (M.N. is a recipient of a Research to Prevent Blindness Stein Innovation Award), the Cure Alzheimer's Fund . The content is solely the responsibility of the authors and does not necessarily represent the official views of the sponsors.

Funding Information:
This project has received funding from the European Research Council (ERC) under the European Union's Horizon 2020 research and innovation programme (grant agreement no. 742112), the Novo Nordisk and the Lundbeck Foundations, Dr. Miriam and Sheldon G. Adelson Medical Research Foundation, the NIH/NINDS/NIA (R01NS100366 and RF1AG057575), the Research to Prevent Blindness Foundation (M.N. is a recipient of a Research to Prevent Blindness Stein Innovation Award), the Cure Alzheimer's Fund. The content is solely the responsibility of the authors and does not necessarily represent the official views of the sponsors.

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