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

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

Publication Details

Journal
The Medicine Forum
Published
2024-09-20
Primary Topic
Magnetic confinement fusion research
Type
article
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article

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

The Medicine Forum
Magnetic confinement fusion research
article

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

article en

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

The Medicine Forum
Openalex Percentile: Top 41%
Magnetic confinement fusion research
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