Scientists pinpoint genetic target with promise for treating many forms
of blindness

Date:
February 17, 2022
Source:
Trinity College Dublin
Summary:
Developing therapies for genetic forms of blindness is extremely
challenging, in part because they vary so widely, but scientists
have now highlighted a target with great promise for treating a
range of these conditions. The scientists have highlighted that a
specific gene (SARM1) is a key driver in the damage that ultimately
leads to impaired vision (and sometimes blindness), and -- in a
disease model -- showed that deleting this gene protects vision
after a chemical kick-starts the chain of dysfunction that mimics
a host of ocular conditions.



FULL STORY ========================================================================== Developing therapies for genetic forms of blindness is extremely
challenging, in part because they vary so widely, but scientists from
Trinity College Dublin have highlighted a target with great promise for treating a range of these conditions.


==========================================================================
The scientists have highlighted that a specific gene (SARM1) is a key
driver in the damage that ultimately leads to impaired vision (and
sometimes blindness), and -- in a disease model -- showed that deleting
this gene protects vision after a chemical kick-starts the chain of
dysfunction that mimics a host of ocular conditions.

This means that therapies targeting suppression of SARM1 activity may
hold the key to effective new options for treating a suite of diseases
that can have a devastating impact on quality of life, and for many of
which there are no treatment options currently available.

The scientists, led by a team from Trinity's School of Genetics and Microbiology, have just published their findings in the International
Journal of Molecular Sciences.

First author on the paper, Laura Finnegan, a PhD Candidate at Trinity,
said: "In response to injury SARM1 contributes to a process that leads to
the degeneration of specialised cells and their axons in the eye. When
this happens it essentially means that the optic nerve can no longer
deliver signals from the eye to the brain.

"Impaired vision and blindness is extremely debilitating for millions
of people across the globe, which is one of the main motivations for
us to seek to better understand the genetic causes and, potentially,
develop life-changing therapies." Jane Farrar, Professor in Trinity's
School of Genetics and Microbiology, senior author on the paper, said:
"Another important finding was that visual function was still preserved
when reassessed four months after SARM1 was deleted, indicating that
the benefits can remain over time. This raises hopes that a targeted
therapy delivered early enough may offer people diagnosed with an ocular neuropathy long-lasting preservation of sight.

"We have a way to go before such a therapy is available but this work represents a significant step, sheds light on the pathway forward and
offers hope that a range of diseases involving the optic nerve -- from maternally inherited conditions such as Leber Hereditary Optic Neuropathy
to the more commonly known glaucoma -- will one day be treatable via
such therapies." The research is the result of collaboration between
Professor Farrar's lab in the School of Genetics and Microbiology and
that of Professor Andrew Bowie's in the School of Biochemistry and
Immunology in the Trinity Biomedical Sciences Institute.

It was funded by the Irish Research Council, Science Foundation Ireland,
the Health Research Board of Ireland and Fighting Blindness Ireland.

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========================================================================== Journal Reference:
1. Laura K. Finnegan, Naomi Chadderton, Paul F. Kenna, Arpad Palfi,
Michael
Carty, Andrew G. Bowie, Sophia Millington-Ward, G. Jane
Farrar. SARM1 Ablation Is Protective and Preserves Spatial
Vision in an In Vivo Mouse Model of Retinal Ganglion Cell
Degeneration. International Journal of Molecular Sciences, 2022;
23 (3): 1606 DOI: 10.3390/ijms23031606 ==========================================================================

Link to news story: https://www.sciencedaily.com/releases/2022/02/220217141220.htm

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