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Fluorescence Lifetime Imaging Ophthalmoscopy (FLIO), A Novel Retinal Mitochondrial Biomarker For Parkinson’s Disease

K. Shivok, E. Affel, M. Alizadeh, T-W. Liang, D. Kremens, R. Sergott (Philadelphia, USA)

Meeting: 2024 International Congress

Abstract Number: 328

Keywords: Mitochondria, Mitochondrial dysfunction

Category: Parkinson's Disease: Non-Motor Symptoms

Objective: Using fluorescence-lifetime ophthalmoscopy (FLIO), we identified retinal mitochondrial changes in Parkinson’s disease (PD) patients compared to controls.

Background: FLIO, a novel non-invasive, in vivo imaging technology, generates fluorescent lifetime decay times in two spectral channels corresponding to short and longer lived retinal chromophores.  This decay data reflects changes within the mitochondrial molecular environment for both the oxidative phosphorylation pathway and ATP production as well as lysosomal and lipofuscin metabolism. Mitochondrial dysfunction is recognized as a major contributor to the pathogenesis of Parkinson’s Disease.

Method: Twenty-seven PD patients of varying stages and duration and nine controls underwent FLIO. Data were analyzed using SPCImage technology. Amplitude-weighted mean fluorescence decay times of the fovea and average decay time of the retina are presented using box-cox transformation followed by a linear regression model with age as a confounding variable.

Results: Three parameters, average total decay time of the retina (u), average total decay of the retina + 1 standard deviation (u + sig), as well as amplitude-weighted mean fluorescence decay time of the fovea ™ were found to be statistically significant (p < 0.05). Differences were found in both long and short spectral channels for both eyes and their corresponding average decay time (u) when compared to controls. Amplitude-weighted mean fluorescence decay time of the fovea for the short spectral channel in the left eye indicated a statistically significant distinction between control and PD cohorts as well. Both channels and their corresponding average decay time when compared to controls displayed an overall right shift towards longer wavelengths, indicating lysosomal lipofuscin dysfunction.

Conclusion: Our data support FLIO as a method of detecting mitochondrial changes in Parkinson’s Disease. We suggest that FLIO may evolve into an objective biomarker for both clinical research and trials for PD. Future work will focus on FLIO as an imaging biomarker to stratify mitochondrial dysfunction in mild, moderate, and severe Parkinson’s Disease.

To cite this abstract in AMA style:

K. Shivok, E. Affel, M. Alizadeh, T-W. Liang, D. Kremens, R. Sergott. Fluorescence Lifetime Imaging Ophthalmoscopy (FLIO), A Novel Retinal Mitochondrial Biomarker For Parkinson’s Disease [abstract]. Mov Disord. 2024; 39 (suppl 1). https://www.mdsabstracts.org/abstract/fluorescence-lifetime-imaging-ophthalmoscopy-flio-a-novel-retinal-mitochondrial-biomarker-for-parkinsons-disease/. Accessed June 15, 2025.
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