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GLAUCOMA
Clinical
Glaucoma affects over 2 million
Americans and over 67 million people worldwide. It is
typically, but not always,
associated with raised pressure in the eye. Normally, fluid
(aqueous humour) is produced in the rear chamber of the
eye, flows through the pupil to the front chamber, where
it drains out through the “canals of Schlemm”.
The aqueous humour provides oxygenation, nutrition and
structural support to the eye.
Raised intraocular pressure (IOP) can occur because of
excessive fluid production, or insufficient drainage. The
raised pressure within the eye may then damage the optic
nerve. Although the raised IOP is a major risk factor for
glaucomatous optic nerve damage, there are other factors
at play. Some patients suffer optic nerve damage and degeneration
with normal IOPs, whilst others continue to experience
optic nerve degeneration despite a normalisation of the
IOP. The causes of glaucoma are largely unknown, although
there is a hereditary component.
The majority of patients do not notice any symptoms until
significant visual loss has occurred. This may be irreversible.
Hence the importance of routine screening for all people
older than 35, particularly if there is a positive family
history.
Source: National
Eye Institute, National
Institutes of Health
The standard therapies
are meiotics, beta blockers, carbonic anhydrase inhibitors
and prostaglandins. Meiotics, such
as pilocarpine, constrict the pupil, with the consequence
that the flow of aqueous humour out of the eye is increased.
Beta blockers and carbonic anhydrase inhibitors decrease
the production of aqueous humour, whereas prostaglandin
analogues (e.g. latanoprost) increase the outflow.
Many of the drugs have side effects, although these tend
to
be non-serious and temporary. Treatment is lifelong.
Some patients additionally require surgery to try and decrease
intraocular pressure.
DanioLabs approach
DanioLabs approach is to both develop
compounds that modulate intraocular pressure, as
well as compounds which have a direct effect on
ganglion cell and optic nerve survival.
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