NMOSD Mitochondrial Fluorescence Correlates with Ganglion Cell Layer Loss Consistent with Retinal Vasculitis

Authors

Francesco Cappellani, MD, Thomas Jefferson UniversityFollow
Daniel M. Markowitz, BS, Thomas Jefferson UniversityFollow
Elizabeth Affel, MS, Thomas Jefferson UniversityFollow
Jose S. Pulido, MD, Thomas Jefferson UniversityFollow
Brian Fernandez, MD, Heidelberg Engineering, Heidelberg, Germany
Robert C. Sergott, MD, Thomas Jefferson UniversityFollow

Document Type

Poster

Publication Date

9-20-2024

Comments

Presented at the 40th Congress of the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS) 2024.

Abstract

Introduction

• Fluorescence lifetime imaging ophthalmoscopy (FLIO, Heidelberg Engineering, Figures 1 and 2), a novel in vivo retinal imaging biomarker, generates fluorescence decay lifetimes in 2 spectral channels corresponding to mitochondrial metabolic processes
• Short Spectral Channel (SSC): 498 – 560 nm Ø Corresponds to flavin adenine dinucleotide (FAD) and oxidative phosphorylation.
• Long Spectral Channel (LSC): 560 – 720nm Ø Corresponds to predominantly lipofuscin and lysosomal function
• Based upon animal experimental models and clinical data, mitochondrial dysfunction has a role in the pathophysiology of NMOSD

Recommended Citation

Cappellani, MD, Francesco; Markowitz, BS, Daniel M.; Affel, MS, Elizabeth; Pulido, MD, Jose S.; Fernandez, MD, Brian; and Sergott, MD, Robert C., "NMOSD Mitochondrial Fluorescence Correlates with Ganglion Cell Layer Loss Consistent with Retinal Vasculitis" (2024). Farber Institute for Neuroscience Staff Papers and Presentations. Paper 6.
https://jdc.jefferson.edu/farberneurospapers/6

Language

English