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| Funder | Swedish Research Council |
|---|---|
| Recipient Organization | Umeå University |
| Country | Sweden |
| Start Date | Jan 01, 2024 |
| End Date | Dec 31, 2027 |
| Duration | 1,460 days |
| Number of Grantees | 10 |
| Roles | Co-Investigator; Principal Investigator |
| Data Source | Swedish Research Council |
| Grant ID | 2023-00355_VR |
Glaucoma is the leading cause of irreversible blindness and affects ~80 million patients worldwide (~100-200,000 in Sweden). Current treatment strategies only target lowering intraocular pressure (IOP). Despite this, >40% of treated patients progress to blindness. Thus, elevated IOP does not fully explain the pathophysiology of glaucoma.
So far, search for a treatment that targets the retina and optic nerve and arrests progression, has a low side effect profile, and is cost-effective has been unsuccessful.Metabolic decline may be a critical, treatable pathogenic component of glaucoma.
An essential metabolite, NAD, declines in the retina and optic nerve in glaucoma animal models and treatment with nicotinamide (NAM; the amide of vitamin B3 and an NAD precursor) robustly prevents glaucomatous neurodegeneration.
Supporting this, NAM is low in the sera of glaucoma patients, and we have demonstrated that NAM can restore visual function in exisiting glaucoma patients in a preliminary clinical trial.
NAM is safe and well-tolerated with an ideal safety profile established over 75-years of clinical use.The aim of this project is to assess NAM as a neuroprotective agent to halt or minimize vision loss in glaucoma patients.
Specifically, this project will:- Establish an adequately powered glaucoma clinical trial for NAM,- Assess beneficial effects of NAM treatment on the quality of life on glaucoma patients,- Assess blood metabolomic profiles of treated and untreated glaucoma patients.
Umeå University
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