Neglected neurotoxicants

Article Abstract:

During the manufacture of synthetic heroin, a small amount of a chemical called MPTP can be produced. MPTP causes symptoms similar to those seen in Parkinson's disease, which became apparent when Parkinson's disease symptoms were reported in drug addicts. This example of how a toxic chemical can poison the nervous system prompted experts to consider whether a variety of disorders of the nervous system may be due to exposure to neurotoxicants, chemicals toxic to the nervous system. A report by the Office of Technology Assessment concluded that only a few chemicals have been tested to see if they affect the nervous system, and that research on neurotoxicants is underfunded. It is known that a large percentage of the chemicals present in pesticides affect the nervous system. Other substances that may be neurotoxic are found in industrial chemicals, food additives, cosmetic ingredients, therapeutic and abused drugs, and substances such as lead, which are naturally occurring. There is evidence that environmental agents may play a role in the increased incidence of amyotrophic lateral sclerosis, or Lou Gehrig's disease, and in Parkinson's disease. The government does not appear to be overly concerned about the hazards which may be posed by neurotoxicants. Regulations which exist are fragmented, and regulatory agencies are poorly coordinated. There are problems in developing regulations, as the effects of the neurotoxicants can vary greatly and the bodily changes that cause neurologic disorders are not understood. It is difficult to test compounds for neurologic effects because of the lack of understanding about the mechanisms of toxicity. There are no available tests which can be done in tissue culture, therefore testing must be performed in animals. Additional research is needed, which means the government must provide funding for research in neurotoxicology. (Consumer Summary produced by Reliance Medical Information, Inc.)

Health aspects, Analysis, Nervous system, Environmental health, Amyotrophic lateral sclerosis, Biochemical toxicology, Toxicology

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Reversal of experimental Parkinsonism by lesions of the subthalamic nucleus

Article Abstract:

Parkinson's disease, a condition characterized by akinesia (cessation or reduction of movement), muscular rigidity, and tremor, is associated with decreased amounts of dopamine (a neurotransmitter) in the basal ganglia, a part of the brain concerned with movement. When this substance is lost, neural activity changes in two groups of neurons (brain cells) that project to the thalamic region called STN (subthalamic nucleus), ultimately leading to reduced neuronal activity in the cerebral cortex (which controls movement). To learn more about the effects of the STN on Parkinson's disease, measurement of STN neurons in two parkinsonian monkeys was performed. In addition, the effects of lesions (damage) to the STN on the monkeys' symptoms were determined. Monkeys treated systemically with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) develop classic parkinsonian symptoms; this model was used. Results showed that injections of ibotenic acid (a toxic substance) into the STN on one side of the brain led to a decrease in STN activity. In addition, a marked reduction in akinesia, rigidity, and tremor on the side opposite the lesion (motor control in the central nervous system is crossed) were observed. The results suggest that akinesia and other symptoms of Parkinson's disease may result from excessive activity of the STN, rather than from the absence of neuronal activity, as has been thought. A discussion is provided of the anatomy of the brain regions involved in Parkinson's disease. Pharmacological agents that inactivate the STN may be effective in treating the disorder. (Consumer Summary produced by Reliance Medical Information, Inc.)

Physiological aspects

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The effect of deprenyl (selegiline) on the natural history of Parkinson's disease

Article Abstract:

Parkinson's disease is a progressive degenerative disease of the brain that causes inhibited movement, tremors, and muscular rigidity. The effects of a chemical that produces the symptoms of Parkinson's disease can be prevented in laboratory animals by treatment with deprenyl, which blocks the activity of certain enzymes. The effectiveness of deprenyl against Parkinson's disease in humans was studied in 54 patients. Deprenyl treatment increased the length of time before another treatment for Parkinson's disease was necessary from an average of 321 days to an average of 549 days. Deprenyl slowed disease progression by an average of 40 to 83 percent.

Research, Evaluation, Antiparkinsonian agents, Selegiline, Antiparkinson agents

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