Exploring the Effects of Non-Thermal Infrared Irradiation on an AlzheimerΓÇÖs Disease Mouse Model

Durham University (2010) Proc Physiol Soc 21, PC34

Poster Communications: Exploring the Effects of Non-Thermal Infrared Irradiation on an AlzheimerΓÇÖs Disease Mouse Model

N. A. Duggett1, S. L. Burroughs1, P. L. Chazot1

1. School of Biological & Biomedical Sciences, Durham University, Durham, United Kingdom.

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Non-thermal infrared (IR) wavelengths (700-1100nm) have been shown to elicit a broad range of physiological effects and therapeutic benefits, including modulation of many cellular processes involved in the progression of ageing1. It has been widely postulated that a primary photoacceptor for IR lies within the mitochondria and stimulation initiates retrograde signalling, enabling mitochondria-nucleus communication, influencing a plethora of cellular processes2,5. Our research focuses on 1072nm, a wavelength at the peak of IR transmission through water and thus high tissue penetrability1. Previously we have reported chronic exposure in vivo significantly improved learning performance in a premature ageing, CD-1 mouse model3. Recent unpublished studies from our laboratory have shown IR1072 treatment reduced Aβ42 expression and plaques in TASTPM Alzheimer’s disease model mice, in a gender-dependent manner. All experiments were performed in accordance with the Animals (Scientific Procedures) Act, 1986. TASTPM (GSK, UK), were exposed to sham or IR1072nm treatment for 6 minutes for 2 successive days, biweekly over 5 months, equipment temperature was continually monitored. Parallel sham treatments were undertaken in replica apparatus which did not emit IR1072nm. (n=3-4 per group) Mice were humanely killed, decapitated, brain tissue dissected, homogenised and subjected to quantitative immunoblotting probing with rabbit anti-HSP27 (Heat Shock Protein-27), HSP70 or HSP105 (1:125, 2 days, 4○C) antibodies, normalised against mouse anti-β-actin (1:3000, overnight, 4○C). Results were quantified using ImageJ to measure optical densitometry. Mitochondria from the brain and liver of non-treated mice were isolated and Complex I and II activity of the respiratory chain measured using the polarographic method4. Data were analysed using a non-parametric Student’s two tailed T-test. (n=3-6 replicates) We have found significant effects in TASTPM mice, with an apparent down-regulation of HSP105 (p<0.001) and HSP70 (p<0.001) in IR treated males and upregulation of HSP70 (p<0.05) in IR treated females but no respective change in HSP105 expression. Preliminary results showed that female TASTPM mice had higher respiratory complex activity and a higher RCI (respiratory control index) than their male counterparts. This may explain sexual dimorphism in HSP70 and Aβ42 expression; increased mitochondrial activity can lead to AP-1 (activator protein-1) induction, which induces transcription factors resulting in DNA synthesis and thus increased protein levels2,5. Further investigation is required to determine whether such high complex activity is maintained or even increased further in IR treated female TASTPM mice to determine the role of the mitochondria in HSP activation.



Where applicable, experiments conform with Society ethical requirements.

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