Hypothesis: Etiologic and Molecular Mechanistic Leads for Sporadic Neurodegenerative Diseases Based on Experience With Western Pacific ALS/PDC

To understand the health impact of long-duration spaceflight, one identical twin astronaut was monitored before, during, and after a 1-year mission onboard the International Space Station; his twin served as a genetically matched ground control. Longitudinal assessments identified spaceflight-specific changes, including decreased body mass, telomere elongation, genome instability, carotid artery distension and increased intima-media thickness, altered ocular structure, transcriptional and metabolic changes, DNA methylation changes in immune and oxidative stress-related pathways, gastrointestinal microbiota alterations, and some cognitive decline postflight. Although average telomere length, global gene expression, and microbiome changes returned to near preflight levels within 6 months after return to Earth, increased numbers of short telomeres were observed and expression of some genes was still disrupted. These multiomic, molecular, physiological, and behavioral datasets provide a valuable roadmap of the putative health risks for future human spaceflight.

DNA damage created by endogenous or exogenous genotoxic agents can exist in multiple forms, and if allowed to persist, can promote genome instability and directly lead to various human diseases, particularly cancer, neurological abnormalities, immunodeficiency and premature aging. To avoid such deleterious outcomes, cells have evolved an array of DNA repair pathways, which carry out what is typically a multiple-step process to resolve specific DNA lesions and maintain genome integrity. To fully appreciate the biological contributions of the different DNA repair systems, one must keep in mind the cellular context within which they operate. For example, the human body is composed of non-dividing and dividing cell types, including, in the brain, neurons and glial cells. We describe herein the molecular mechanisms of the different DNA repair pathways, and review their roles in non-dividing and dividing cells, with an eye toward how these pathways may regulate the development of neurological disease. Published by Elsevier B.V.

Environmental pollution from hazardous waste materials, organic pollutants and heavy metals, has adversely affected the natural ecosystem to the detriment of man. These pollutants arise from anthropogenic sources as well as natural disasters such as hurricanes and volcanic eruptions. Toxic metals could accumulate in agricultural soils and get into the food chain, thereby becoming a major threat to food security. Conventional and physical methods are expensive and not effective in areas with low metal toxicity. Bioremediation is therefore an eco-friendly and efficient method of reclaiming environments contaminated with heavy metals by making use of the inherent biological mechanisms of microorganisms and plants to eradicate hazardous contaminants. This review discusses the toxic effects of heavy metal pollution and the mechanisms used by microbes and plants for environmental remediation. It also emphasized the importance of modern biotechnological techniques and approaches in improving the ability of microbial enzymes to effectively degrade heavy metals at a faster rate, highlighting recent advances in microbial bioremediation and phytoremediation for the removal of heavy metals from the environment as well as future prospects and limitations. However, strict adherence to biosafety regulations must be followed in the use of biotechnological methods to ensure safety of the environment.