Pete Williams "From bench to bedside and back again: Targeting NAD for neuroprotection in glaucoma"
- When Oct 24, 2025 from 12:00 PM to 01:15 PM (Europe/Berlin / UTC200)
- Where Auditorium Angelo Maramai
- Contact Name Alessia Indrieri
- Contact Phone 08119230659
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- https://www.tigem.it/newsroom/seminars/pete-williams-from-bench-to-bedside-and-back-again-targeting-nad-for-neuroprotection-in-glaucoma
- Pete Williams "From bench to bedside and back again: Targeting NAD for neuroprotection in glaucoma"
- 2025-10-24T12:00:00+02:00
- 2025-10-24T13:15:00+02:00
Pete Williams
Ulla and Ingemar Dahlberg Professor in Vision Science
Research Group Leader – Glaucoma
Dept. of Clinical Neuroscience
Division of Eye and Vision
Karolinska Institutet & St. Erik Eye Hospital
Stockholm, Sweden
Short CV
Abstract
Pete Williams will discuss targeting NAD metabolism for neuroprotection in glaucoma, a progressive neurodegenerative disease leading to retinal ganglion cell (RGC) loss and irreversible vision impairment. The work will highlight aging-related decline in NAD and mitochondrial dysfunction in RGCs as critical contributors to glaucoma pathogenesis. Preclinical studies demonstarte that boosting NAD levels, via nicotinamide supplementation or gene therapy targeting NMNAT2, robustly protects RGCs and improves visual function in animal models and preliminary human trials. Ongoing clinical trials aim to validate nicotinamide's therapeutic potential. The lab is furthering this work through drug discovery and development efforts focusing on stabilizing and enhancing NMNAT2 for glaucoma treatment. This multidisciplinary approach offers promising avenues to complement existing intraocular pressure-lowering therapies by directly enhancing neuronal metabolic resilience and axonal health.
Ulla and Ingemar Dahlberg Professor in Vision Science
Research Group Leader – Glaucoma
Dept. of Clinical Neuroscience
Division of Eye and Vision
Karolinska Institutet & St. Erik Eye Hospital
Stockholm, Sweden
Short CV
Abstract
Pete Williams will discuss targeting NAD metabolism for neuroprotection in glaucoma, a progressive neurodegenerative disease leading to retinal ganglion cell (RGC) loss and irreversible vision impairment. The work will highlight aging-related decline in NAD and mitochondrial dysfunction in RGCs as critical contributors to glaucoma pathogenesis. Preclinical studies demonstarte that boosting NAD levels, via nicotinamide supplementation or gene therapy targeting NMNAT2, robustly protects RGCs and improves visual function in animal models and preliminary human trials. Ongoing clinical trials aim to validate nicotinamide's therapeutic potential. The lab is furthering this work through drug discovery and development efforts focusing on stabilizing and enhancing NMNAT2 for glaucoma treatment. This multidisciplinary approach offers promising avenues to complement existing intraocular pressure-lowering therapies by directly enhancing neuronal metabolic resilience and axonal health.