Hormesis may result when mild repetitive stress increases cellular defense against diverse injuries. This process may also extend in vitro cellular proliferative life span as well as delay and reverse some of the age-dependent changes in both replicative and non-replicative cells. This study evaluated the potential hormetic effect of non-thermal repetitive electromagnetic field shock (REMFS) and its impact on cellular aging and mortality in primary human T lymphocytes and fibroblast cell lines. Unlike previous reports employing electromagnetic radiation, this study used a long wave length, low energy, and non-thermal REMFS (50MHz/0.5W) for various therapeutic regimens. The primary outcomes examined were age-dependent morphological changes in cells over time, cellular death prevention, and stimulation of the heat shock response. REMFS achieved several biological effects that modified the aging process. REMFS extended the total number of population doublings of mouse fibroblasts and contributed to youthful morphology of cells near their replicative lifespan. REMFS also enhanced cellular defenses of human T cells as reflected in lower cell mortality when compared to non-treated T cells. To determine the mechanism of REMFS-induced effects, analysis of the cellular heat shock response revealed Hsp90 release from the heat shock transcription factor (HSF1). Furthermore, REMFS increased HSF1 phosphorylation, enhanced HSF1-DNA binding, and improved Hsp70 expression relative to non-REMFS-treated cells. These results show that non-thermal REMFS activates an anti-aging hormetic effect as well as reduces cell mortality during lethal stress. Because the REMFS configuration employed in this study can potentially be applied to whole body therapy, prospects for translating these data into clinical interventions for Alzheimer's disease and other degenerative conditions with aging are discussed.

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Late-onset Alzheimer’s disease (LOAD) is the most common neurodegenerative disorder in older adults, affecting over 50% of those over age 85. Aging is the most important risk factor for the development of LOAD. Aging is associated with the decrease in the ability of cells to cope with cellular stress, especially protein aggregation. Here we will describe how the process of aging affects pathways that control the processing and degradation of abnormal proteins including amyloid-β (Aβ). Genetic association studies in LOAD have successfully identified a large number of genetic variants involved in the development of the disease. However, there is a gap in understanding the interconnections between these pathomolecular events that prevent us from discovering therapies. We will compile pertinent links to elucidate how the biology of aging affects the sequence of events in the development of LOAD. Specifically, in this review we analyze the molecular-pathologic-clinical correlations of the aging process, the HSF1 and FOXO family pathways, Aβ toxicity, Aβ degradation, and the different clinical stages of LOAD.

The impact of the electromagnetic waves (EM) on human neurons (HN) has been under investigation for decades, in efforts to understand the impact of cell phones (radiation) on human health, or radiation absorption by HN for medical diagnosis and treatment. Research issues including the wave frequency, power intensity, reflections and scattering, and penetration depths are of important considerations to be incorporated into the research study. In this study, computer simulation for the EM exposure to HN was studied for the purpose of determining the upper limits of the electric and magnetic field intensities, power consumption, reflections and transmissions, and the change in temperature resulting from the power absorption by human neurons. Both high frequency structural simulators (HFSS) from ANSYS software, and COMSOL multi-physics were used for the simulation of the EM transmissions and reflections, and the temperature profile within the cells, respectively. For the temperature profile estimation, the study considers an electrical source of 0.5 watt input power, 64 MHz. The EM simulation was looking into the uniformity of the fields within the sample cells. The size of the waveguide was set to be appropriate for a small animal model to be conducted in the future. The incident power was fully transmitted throughout the waveguide, and less than 1% reflections were observed from the simulation. The minimum reflected power near the sample under investigation was found to be with negligible reflected field strengths. The temperature profile resulting from the COMSOL simulation was found to be near 0.25 m°K, indicating no change in temperature on the neuro cells under the EM exposure. The paper details the simulation results for the EM response determined by HFSS, and temperature profile simulated by COMSOL.