Management of glaucoma as a neurodegenerative disease
File(s)
Author(s)
Hill, Daniel
Pei, Kun
Cordeiro, Maria Francesca
Type
Journal Article
Abstract
The pathology of glaucoma has long been known to be linked with raised intraocular pressure (IOP), generally resulting from impaired outflow of aqueous humor from the anterior chamber of the eye. Raised IOP results in mechanical disturbance of the lamina cribrosa, the opening in the posterior of the eye through which the optic nerve passes, in turn, damaging retinal ganglion cells (RGCs; whose axons form the optic nerve), resulting in cell death. The patient typically suffers loss of vision that is insidiously masked from perception until later stages of the disease, due to compensatory visual mechanisms. As a result, substantial and irreversible vision loss can easily occur prior to both symptoms and diagnosis of the disease [Citation1].
To the present day, clinical management of glaucoma has been achieved through the reduction of IOP. As the only clinically modifiable risk factor in glaucoma, it is unsurprising that a diverse suite of therapeutic agents has been developed to control IOP, primarily through reducing production, or increasing outflow of aqueous humor [Citation2]. While this approach is effective in many cases of glaucoma, understanding of the underlying pathology of the disease has grown over recent decades, so much so that elevated IOP is no longer a diagnostic criterion. This shift is in part due to the high prevalence of ‘normal tension glaucoma’ (NTG), presenting in a substantial subset of glaucoma cases, whereby glaucomatous pathology is detected despite an IOP that is within normal bounds (below 21 mmHg) [Citation3]. While IOP management remains an effective therapeutic pathway in NTG, the existence of NTG highlights the limitations of a purely ocular, pressure-centric model of glaucoma.
To the present day, clinical management of glaucoma has been achieved through the reduction of IOP. As the only clinically modifiable risk factor in glaucoma, it is unsurprising that a diverse suite of therapeutic agents has been developed to control IOP, primarily through reducing production, or increasing outflow of aqueous humor [Citation2]. While this approach is effective in many cases of glaucoma, understanding of the underlying pathology of the disease has grown over recent decades, so much so that elevated IOP is no longer a diagnostic criterion. This shift is in part due to the high prevalence of ‘normal tension glaucoma’ (NTG), presenting in a substantial subset of glaucoma cases, whereby glaucomatous pathology is detected despite an IOP that is within normal bounds (below 21 mmHg) [Citation3]. While IOP management remains an effective therapeutic pathway in NTG, the existence of NTG highlights the limitations of a purely ocular, pressure-centric model of glaucoma.
Date Issued
2026-02-26
Date Acceptance
2026-02-17
Citation
Neurodegenerative Disease Management, 2026, pp.1-3
ISSN
1758-2024
Publisher
Taylor and Francis Group
Start Page
1
End Page
3
Journal / Book Title
Neurodegenerative Disease Management
Copyright Statement
Copyright © 2026 Informa UK Limited, trading as Taylor & Francis Group This is the author’s accepted manuscript made available under a CC-BY licence in accordance with Imperial’s Research Publications Open Access policy (www.imperial.ac.uk/oa-policy)
License URL
Identifier
https://www.ncbi.nlm.nih.gov/pubmed/41744356
Subjects
AO
AO-OCT
DARC
Glaucoma
Neurodegeneration
Neuroprotection
OCT
RGC
cSLO
Publication Status
Published online
Coverage Spatial
England
Date Publish Online
2026-02-26