Review of the evidence on the influence of Wi-Fi 2.4 GHz radiation on oxidative stress and its possible relationship with Alzheimer’s disease.

A new study by a Peruvian research group examined the effects of 2.4 GHz Wi-Fi radiation, with a particular focus on its role in oxidative stress and its potential link to Alzheimer's disease (AD). Alzheimer's disease is multifactorial, developing as a result of the complex interaction of genetic, environmental, and lifestyle factors.

The authors conducted a literature search in accordance with PRISMA guidelines. The review addressed 3 questions:

1) How does exposure to 2.4 GHz electromagnetic fields affect gene expression related to oxidative stress response, genomic stability, metabolism, and cellular regulation?

2) How does the regulation of oxidative stress and protein homeostasis influence the progression of neurodegeneration in Alzheimer's disease?

3) Can genes associated with Alzheimer's disease interact functionally with genes involved in DNA repair, metabolism, and cellular regulation?

A total of 49 studies were used to synthesize and map genetic relationships. Several genes, including APOE and GSK3B, have been directly linked to Alzheimer's disease (AD). Beyond their role in AD pathogenesis, genes such as MAGED4, HSPB8, HSPB6, HSF1, HSPA4, HSPB1, and MAPKAPK5 play a crucial role in the cellular response to oxidative stress, which is a key factor in the pathogenesis of various diseases. These genes contribute to cell protection by regulating protein homeostasis, stabilizing misfolded proteins and preventing apoptosis induced by reactive oxygen species (ROS). This highlights their importance in preventing diseases related to oxidative stress. Furthermore, exposure to electromagnetic fields (EMFs) at a frequency of 2.4 GHz has been shown to alter the expression of several genes associated with DNA replication, cellular homeostasis, and metabolism. These include POLD4 and FEN1, both of which are essential for DNA replication and repair and whose altered expression could compromise genomic stability. In addition, EXOG, which is involved in mitochondrial DNA repair, exhibits changes that suggest a potential disruption to mitochondrial function. Taken together, these findings suggest that exposure to Wi-Fi radiation can significantly alter genomic stability, metabolism, and cellular regulation. Genes associated with Alzheimer's disease, including ABCA7, PICALM, CLU, TREM2, APOE, SORL1, GSK3B, and PRNP, intersect with HSP27, HSPB1, HSP70, and HSPA4. The latter genes are all part of the "heat shock protein (HSP)" family and regulate oxidative stress. The genes involved in regulating Alzheimer's disease also intersect with POLD4, FEN1, and EXOG, among others, which showed reduced expression after exposure to 2.4 GHz Wi-Fi radiation.

Recent research on Alzheimer's disease (AD) has identified several genes that contribute to its pathogenesis. These genes are located in a highly dynamic biological environment in which oxidative stress plays a central role in the cell damage associated with neurodegeneration. The activation of heat shock proteins (HSPs), such as HSPB1 and HSPA4, is of particular interest in Alzheimer's disease because these proteins protect cells from oxidative stress. Several studies suggest that exposure to Wi-Fi radiation can alter the expression of genes involved in DNA replication and repair processes. This indicates that exposure to this frequency of RF radiation could compromise genomic stability and mitochondrial function. While the authors could not find direct evidence of a link between Wi-Fi exposure and AD, the indirect link via oxidative stress is concerning and warrants further investigation. (AT)