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. 2018 Feb 2:4:54-63.
doi: 10.1016/j.trci.2017.12.003. eCollection 2018.

Neuroprotective effect of a new photobiomodulation technique against Aβ25-35 peptide-induced toxicity in mice: Novel hypothesis for therapeutic approach of Alzheimer's disease suggested

Affiliations

Neuroprotective effect of a new photobiomodulation technique against Aβ25-35 peptide-induced toxicity in mice: Novel hypothesis for therapeutic approach of Alzheimer's disease suggested

Guillaume Blivet et al. Alzheimers Dement (N Y). .

Abstract

Introduction: Photobiomodulation was assessed as a novel treatment of Alzheimer's disease (AD) by the use of a new device RGn500 combining photonic and magnetic emissions in a mouse model of AD.

Methods: Following the injection of amyloid β 25-35 peptide in male Swiss mice, RGn500 was applied once a day for 7 days either on the top of the head or the center of abdomen or both.

Results: RGn500 daily application for 10 min produced a neuroprotective effect on the neurotoxic effects of amyloid β 25-35 peptide injection when this type of photobiomodulation was applied both on the head and on the abdomen. Protection was demonstrated by memory restoration and on the normalization of key markers of AD (amyloid β 1-42, pTau), oxidative stress (lipid peroxidation), apoptosis (Bax/Bcl2) and neuroinflammation.

Discussion: RGn500 displays therapeutic efficacy similar to other pharmacological approaches evaluated in this model of AD.

Keywords: Alzheimer’s disease; Amyloid β; Electromagnetic; LLLT; Magnetic; Memory; Neurodegenerescence; Neuroinflammation; Oxidative stress; Phosphorylated tau; Photobiomodulation; Photonic.

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Figures

Fig. 1
Fig. 1
Effect of RGn500 treatment on Aβ25–35 (AB25–35)–induced deficits in the spontaneous alternation test. Different times of exposure, the frequency (once a day [o.d.] or twice a day [b.i.d.]) (A), and the mode of delivery with exposure of head alone (at 10 Hz), of abdomen alone (at 1000 Hz), or of both body parts (h/a) (B) were examined. Data are presented as mean ± SEM. ∗∗P < .01, ***P < .001 versus Sc Aβ (Sc.AB) group; ##P < .01, ###P < .001 versus Aβ25–35 group. n = 12–21 per group. Abbreviations: Aβ25–35, amyloid β peptide 25–35; SEM, standard error of mean.
Fig. 2
Fig. 2
Effect of RGn500 treatment on Aβ25–35 (AB25–35)–induced deficits in the step-through latency (A and C) and the escape latency (B and D) in the passive avoidance task. Different times of exposure, the frequency (once a day [o.d.] or twice a day [b.i.d.]), and the mode of delivery with exposure of head alone (at 10 Hz), of abdomen alone (at 1000 Hz), or of both body parts (h/a) were examined. Data are presented as mean ± SEM. ***P < .001 versus Sc Aβ (Sc.AB) group; ##P < .01, ###P < .001 versus Aβ25–35 group. n = 12–21 per group. Abbreviations: Aβ25–35, amyloid β peptide 25–35; SEM, standard error of mean.
Fig. 3
Fig. 3
Effect of RGn500 treatment on Aβ25–35 (AB25–35)–induced increase of lipid peroxidation. Different times of exposure, the frequency (once a day [o.d.] or twice a day [b.i.d.]) (A), and the mode of delivery with exposure of head alone (at 10 Hz), of abdomen alone (at 1000 Hz), or of both body parts (h/a) (B) were examined. Data are presented as mean ± SEM. *P < .05, ***P < .001 versus Sc Aβ (Sc.AB) group; ###P < .001 versus Aβ25–35 group. n = 6 per group. Abbreviations: Aβ25–35, amyloid β peptide 25–35; SEM, standard error of mean.
Fig. 4
Fig. 4
Effect of RGn500 treatment on Aβ25–35 (AB25-35)–induced increase of inflammatory processes, GFAP (A, B), IL-1β (IL-1b) (C), TNFα (TNF alpha) (D, E), and IL6 (IL-6) (F). Different times of exposure, the frequency (once a day [o.d.] or twice a day [b.i.d.]), and the mode of delivery with exposure of head alone (at 10 Hz), of abdomen alone (at 10 Hz), or of both body parts (h/a) were examined. Data are presented as mean ± SEM. *P < .05, **P < .01, ***P < .001 versus Sc Aβ (Sc.AB) group; #P < .05, ##P < .01, ###P < .001 versus Aβ25–35 group. n = 6 per group. Abbreviations: Aβ25–35, amyloid β peptide 25–35; GFAP, glial fibrillary protein; IL-1β, interleukin 1β; IL-6, interleukin 6; SEM, standard error of mean; TNFα, tumor necrosis factor.
Fig. 5
Fig. 5
Effect of RGn500 treatment on Aβ25–35–induced activation of astrocytes (A–C, and G) and microglia (D–F, and H). Exposure was once a day of both the head and abdomen for 10 minutes at 10 Hz on both body parts. **P < .01 versus Sc.Aβ (Sc.AB) group; ***P < .001 versus Sc AB group; ###P < .001 versus Aβ25–35 (AB25–35) group. Abbreviation: Aβ25–35, amyloid β peptide 25–35.
Fig. 6
Fig. 6
Effect of RGn500 on Aβ25–35 (AB25–35)–induced increase of Bax and Bcl2 (A–C), Aβ1-42 (AB1–42) (D) and pTau-Thr181 (E). Exposure was once a day of both the head and abdomen for 10 minutes at 10 Hz on both body parts. Data are mean ± SEM. *P < .05, ***P < .001 versus Sc Aβ (Sc.AB) group; ###P < .001 versus Aβ25–35 (AB25–35) group. n = 6 per group. Abbreviations: Aβ25–35, amyloid β peptide 25–35; SEM, standard error of mean.

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