Paediatrics (RCH) - Research Publications

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Author: Bui, Bang ×

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    Non-invasive in vivo hyperspectral imaging of the retina for potential biomarker use in Alzheimer's disease
    Hadoux, X ; Hui, F ; Lim, JKH ; Masters, CL ; Pebay, A ; Chevalier, S ; Ha, J ; Loi, S ; Fowler, CJ ; Rowe, C ; Villemagne, VL ; Taylor, EN ; Fluke, C ; Soucy, J-P ; Lesage, F ; Sylvestre, J-P ; Rosa-Neto, P ; Mathotaarachchi, S ; Gauthier, S ; Nasreddine, ZS ; Arbour, JD ; Rheaume, M-A ; Beaulieu, S ; Dirani, M ; Nguyen, CTO ; Bui, B ; Williamson, R ; Crowston, JG ; van Wijngaarden, P (NATURE PUBLISHING GROUP, 2019-09-17)
    Studies of rodent models of Alzheimer's disease (AD) and of human tissues suggest that the retinal changes that occur in AD, including the accumulation of amyloid beta (Aβ), may serve as surrogate markers of brain Aβ levels. As Aβ has a wavelength-dependent effect on light scatter, we investigate the potential for in vivo retinal hyperspectral imaging to serve as a biomarker of brain Aβ. Significant differences in the retinal reflectance spectra are found between individuals with high Aβ burden on brain PET imaging and mild cognitive impairment (n = 15), and age-matched PET-negative controls (n = 20). Retinal imaging scores are correlated with brain Aβ loads. The findings are validated in an independent cohort, using a second hyperspectral camera. A similar spectral difference is found between control and 5xFAD transgenic mice that accumulate Aβ in the brain and retina. These findings indicate that retinal hyperspectral imaging may predict brain Aβ load.
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    Increase in mitochondrial DNA mutations impairs retinal function and renders the retina vulnerable to injury
    Kong, YXG ; Van Bergen, N ; Trounce, IA ; Bui, BV ; Chrysostomou, V ; Waugh, H ; Vingrys, A ; Crowston, JG (WILEY, 2011-08)
    Mouse models that accumulate high levels of mitochondrial DNA (mtDNA) mutations owing to impairments in mitochondrial polymerase γ (PolG) proofreading function have been shown to develop phenotypes consistent with accelerated aging. As increase in mtDNA mutations and aging are risk factors for neurodegenerative diseases, we sought to determine whether increase in mtDNA mutations renders neurons more vulnerable to injury. We therefore examined the in vivo functional activity of retinal neurons and their ability to cope with stress in transgenic mice harboring a neural-targeted mutant PolG gene with an impaired proofreading capability (Kasahara, et al. (2006) Mol Psychiatry11(6):577-93, 523). We confirmed that the retina of these transgenic mice have increased mtDNA deletions and point mutations and decreased expression of mitochondrial oxidative phosphorylation enzymes. Associated with these changes, the PolG transgenic mice demonstrated accelerated age-related loss in retinal function as measured by dark-adapted electroretinogram, particularly in the inner and middle retina. Furthermore, the retinal ganglion cell-dominant inner retinal function in PolG transgenic mice showed greater vulnerability to injury induced by raised intraocular pressure, an insult known to produce mechanical, metabolic, and oxidative stress in the retina. These findings indicate that an accumulation of mtDNA mutations is associated with impairment in neural function and reduced capacity of neurons to resist external stress in vivo, suggesting a potential mechanism whereby aging central nervous system can become more vulnerable to neurodegeneration.