IntroductionPhotobiomodulation 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.MethodsFollowing 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.ResultsRGn500 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.DiscussionRGn500 displays therapeutic efficacy similar to other pharmacological approaches evaluated in this model of AD.

Background: Recent innovative non-pharmacological interventions and neurostimulation devices have shown potential for application in the treatment of Alzheimer’s disease (AD). These include photobiomodulation (PBM) therapy. Objective: This pilot study assesses the safety, compliance with, and efficacy of a brain-gut PBM therapy for mild-to-moderate AD patients. Methods: This double-blind, randomized, monocentric sham-controlled study started in 2018 and ended prematurely in 2020 due to the COVID-19 pandemic. Fifty-three mild-to-moderate AD patients were randomized, 27 in the PBM group and 26 in the sham group. All patients had 40 treatment sessions lasting 25 min each over 8 weeks and were followed for 4 weeks afterwards. Compliance with the treatment was recorded. Safety was assessed by recording adverse events (AEs), and efficacy was evaluated using neuropsychological tests. Results: The PBM therapy proved to be safe in regard to the number of recorded AEs (44% of the patients), which were balanced between the PBM and sham groups. AEs were mainly mild, and no serious AEs were reported. The majority of the patients (92.5%) were highly compliant, which confirms the feasibility of the PBM treatment. Compared to the sham patients, the PBM patients showed higher ADAS-Cog comprehension sub-scores and forward verbal spans, and lower TMT-B execution times, which suggests an improvement in cognitive functions. Conclusion: This study demonstrates the tolerability of and patient compliance with a PBM-based treatment for mild-to-moderate AD patients. It highlights encouraging efficacy trends and provides insights for the design of the next phase trial in a larger AD patient sample.

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Quantitative phase microscopies (QPMs) enable label-free, non-invasive observation of living cells in culture, for arbitrarily long periods of time. One of the main benefits of QPMs compared with fluorescence microscopy is the possibility to measure the dry mass of individual cells or organelles. While QPM dry mass measurements on neural cells have been reported this last decade, dry mass measurements on their neurites has been very little addressed. Because neurites are tenuous objects, they are difficult to precisely characterize and segment using most QPMs. In this article, we use cross-grating wavefront microscopy (CGM), a high-resolution wavefront imaging technique, to measure the dry mass of individual neurites of primary neurons in vitro. CGM is based on the simple association of a cross-grating positioned in front of a camera, and can detect wavefront distortions smaller than a hydrogen atom (∼0.1 nm). In this article, an algorithm for dry-mass measurement of neurites from CGM images is detailed and provided. With objects as small as neurites, we highlight the importance of dealing with the diffraction rings for proper image segmentation and accurate biomass measurements. The high precision of the measurements we obtain using CGM and this semi-manual algorithm enabled us to detect periodic oscillations of neurites never observed before, demonstrating the sufficient degree of accuracy of CGM to capture the cell dynamics at the single neurite level, with a typical precision of 2%, i.e., 0.08 pg in most cases, down to a few fg for the smallest objects.

carnitine, coenzyme Q10, polyphenols, ginkgo biloba, long chain polyunsaturated fatty acids -PUFAs) have been devoted a lot of attention [10,11].In this paper we investigate the neuroprotective efficacy of docosahexaenoic acid (DHA), glutathione (GSH), phosphatidylcholine (PC), curcumin (CUR) and resveratrol (RES) given alone or in combination for thirty consecutive days as a preventive treatment in a well recognized mouse model of AD. This model consists in a unique intracerebroventricular (i.c.v.) injection of oligomeric amyloid-beta peptide 25-35 (Aβ 25-35 ) in mice [12] which is able to mimic both cognitive impairment and associated neuronal degeneration. Though Aβ1-40/42 peptides are considered as the major protagonists in the pathology, other small oligomeric fragments have been identified and among those, the highly toxic one is Aβ 25-35 [13,14] which is also endogenously present in AD human brain [15].