Deterioration of skeletal muscle mass and impaired muscle function can occur secondarily following loss of the nerve endings that connect to the muscle. Traumatic injuries and several classes of toxic chemicals (such as nerve gases, certain pesticides, and the industrial chemical acrylamide) target and damage the nerve's axon innervating the muscle, resulting in muscle wasting. Acrylamide is a well-established synthetic neurotoxic chemical agent used in various industries (paper and water purification) since the early 1950s. Repeated exposures to laboratory animals produce a well-established model of axon loss in humans. Acrylamide also forms in carbohydrate-rich foods when cooked to high temperatures, but work performed by CROET Director Dr. Peter Spencer was used by the World Health Organization to demonstrate a low neurotoxic risk among consumers. This was based on studies to determine levels of acrylamide needed to induce axon degeneration. While the levels of human exposure from consumption of these food sources appear to be well below those which cause neurotoxicity, Dr. Bruce Gold recently found that daily injections of the drug FK506 (tacrolimus) to rats also injected with acrylamide dramatically reduce axon loss. Moreover, FK506-treated animals do not develop the functional signs of neurotoxicity. These results may lead to the development of new drugs to protect against axon loss and preserve skeletal muscle function.