Watching synchronous mitochondrial respiration in the retina and its instability in a mouse model of macular degeneration.

Affiliation

Kaynezhad P(1), Tachtsidis I(2), Aboelnour A(3), Sivaprasad S(1), Jeffery G(4).
Author information:
(1)Institute of Ophthalmology, University College London, London, EC1V 9EL, UK.
(2)Department of Medical Physics and Biomedical Engineering, University College London, London, WC1E 6BT, UK.
(3)Histology and Cytology Department, Faculty of Veterinary Medicine, Damanhour University, Damanhour, Egypt.
(4)Institute of Ophthalmology, University College London, London, EC1V 9EL, UK. [Email]

Abstract

Mitochondrial function declines with age and in some diseases, but we have been unable to analyze this in vivo. Here, we optically examine retinal mitochondrial function as well as choroidal oxygenation and hemodynamics in aging C57 and complement factor H (CFH-/-) mice, proposed models of macular degeneration which suffer early retinal mitochondrial decline. In young C57s mitochondrial populations respire in coupled oscillatory behavior in cycles of ~ 8 min, which is phase linked to choroidal oscillatory hemodynamics. In aging C57s, the oscillations are less regular being ~ 14 min and more dissociated from choroidal hemodynamics. The mitochondrial oscillatory cycles are extended in CFH-/- mice being ~ 16 min and are further dissociated from choroidal hemodynamics. Mitochondrial decline occurs before age-related changes to choroidal vasculature, hence, is the likely origin of oscillatory disruption in hemodynamics. This technology offers a non-invasive technique to detect early retinal disease and its relationship to blood oxygenation in vivo and in real time.