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NIEHS to Fund New Marker Studies

By a GenomeWeb staff reporter

NEW YORK (GenomeWeb News) – The National Institute of Environmental Health Sciences sees an "urgent need" for new ways to detect mitochondrial dysfunction, which is associated with a number of major diseases, and has committed $2.5 million this year to fund research into biomarkers for such dysfunctions caused by the environment.

NIEHS said in a new request for applications that it will fund between six and eight research efforts to seek new markers for early mitochondrial dysfunction that results from environmental exposures or stressors.

Mitochondria are known to be targeted by a number of environmental compounds such as pesticides and industrial chemicals, and mitochondrial dysfunction is associated with chronic diseases, such as Type II diabetes, metabolic syndrome, neurodegenerative diseases, blindness, cardiovascular disease, and cancer. However, little is known about how disease and dysfunction may be linked to environmental exposures, and there is a need for tools to measure early markers in humans, according to NIEHS.

Reliable and informative markers of early mitochondrial dysfunction will enhance knowledge about environmentally induced mitochondrial toxicity and disease and could enable preventions and interventions in the subclinical phases of diseases.

The aim of these grants is to use animals and other experimental models to identify targets of environmental stressors; to understand the effects of mitochondrial toxicants between target and surrogate tissues; to provide more understanding of the role of genetics and environment on these interactions; to set standards that could be used to determine the best or most widely accepted measures that signal mitochondrial function; and to develop candidate markers that will be used to develop early biomarkers of dysfunction in human population studies that link exposure to disease.

These NIEHS grants will fund studies that develop gene expression, protein, metabolomic, or biochemical signatures for dysfunction; develop markers of mitochondrial effects; and improving methods for detecting mtDNA mutations and rearrangements induced by environmental stressors, among others.

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