Neurons to provide potential insight into cellular cascades that, by exposure to ELF-EMF, may lead towards neurodegeneration. ELF-EMFs are a form of energy, characterized by wavelength or frequency, that are associated with the use of electrical power that generates a magnetic field at a frequency of 50 Hz and a flux density that primarily ranges between 0.2 and 5 mT. The magnetic flux density selected for our study, 1 mT, is 2- and 10fold the reference levels proposed by the European Community for occupational and general public exposure, respectively. This 1 mT flux density is one of the most studied intensities in medical research focused to elucidate the biological actions of ELF-EMF, consequent to its human translational relevance as during recent years there has been heightened public concern of the impact of ELF-EMFs, associated with both industrial and domesitic use, on human health and welfare. Epidemiological studies have highlighted childhood leukemias, adult primary brain tumors as well as breast cancer, the potential for miscarrage and neurodegenerative disorders. In large part, past studies have been fraught by limited exposure assessment and other methodological limitations, making ELF-EMF epidemiological data interesting but difficult to interpret and then act upon. Whereas the occurrence of some chronic diseases are relatively uncommon and have long latency periods for known risk factors, for others – all be they abundant – their etiologies remain poorly understood, which confounds the observation of potential associations, particularly when relying on mortality records. Nevertheless, the World Health Organization and International Programme on Chemical Safety have issued precautions against ELF-EMFs, resulting in exposure level limits being recommended. In parallel with this, there has been increased focus to understand potential mechanisms via which ELF-EMFs may mediate their actions at a cellular level to guide future epidemiological and in vivo research. The etiology of neurodegenerative diseases is most often multifactorial, and genetic polymorphisms, increasing age as well as environmental cues are primary risk factors. Although different neuronal cell populations are affected across diverse neurodegenerative disorders, hallmark protein modification is a common feature that supports both differential disease diagnosis and provides a mechanistic basis to gauge disease progression. It is becoming increasingly clear that, particularly for chronic neurodegenerative disorders occurring late in life, a complex combination of risk factors can initiate disease development and modify proteins with physiological functions into ones with pathological roles via a number of defined mechanisms. A common denominator in the occurrence of diverse pathogenic mechanisms is oxidative stress accompanied by redox dysregulation, which have a role in metabolic and mitochondrial dysfunction, excitoxicity, calcium handling impairment, glial cell dysfunction and neuroinflammation. Each of these can influence one OSI-774 183319-69-9 another at multiple different levels, and hence oxidative stress can both be secondary to them as well as have a primary part in their initiation.