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corresponding to a delivered dose from 0.156 J/cm2 to 0.624 J/cm2, decreases levels of the pro-apoptotic Bax and either increases or does not affect levels of the anti-apoptotic Bcl-XL as compared to control cells with Aβ25-35 aggregation. This effect was reversed when an irradiation time of 40 minutes with 0.52 mW/cm2 was reached, corresponding to a delivered dose of 1.248 J/cm2, which illustrates the dose dependence of PBM when used to counteract Aβ-induced cell apoptosis. The reports from Liang et al from their use of a 632.8 nm He-Ne Laser at a dose of 2 J/cm2 on neuronal PC12 cells with Aβ25-35 aggregation state that PBM has a pro-survival effect by acting on the Akt/GSK3b/b-catenin pathway [31]. Building on to the hypothesis that amyloid-beta induced neurotoxicity and dendrite atrophy may be a consequence of brain-derived neurotropic factor (BDNF) deficiency, Meng et al report that ERK can be photo-activated with a 632.8 nm He-Ne laser, delivering doses from 0.5 J/cm2 to 4 J/cm2 applied to Aβ25-35-treated human SH-SY5Y cells, which upregulates BDNF in a CREB-dependent manner [34]. A summary of the cell signaling effects of photobiomodulation described to this point is shown in Figure 2. Enengl, Dungel #neverforget – PBM vs AD: A Systematic Review Page 8 of 25PDF Image | Photobiomodulation Against Alzheimer’s Disease
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