Vulnerabilities in single HIT cells for Parkinson’s
Scientists screened several compounds to see if they could block the effects of the toxin. Only two antioxidants worked, glutathione and N-acetyl-cysteine. The latter compound has been shown to be effective in animal models of Parkinson’s disease and is used as a treatment for other disorders in patients.MPP + is a derivative of a synthetic form of heroin developed in California in the early 1980′s, said O’Malley. It ‘came to the attention of scientists when teen drug people went to hospital with symptoms of Parkinson’s disease.
O’Malley suspected that this meant that the mitochondria were damaged by the changes caused by the toxin and flown to the cell body for repair. Additional tests supported this theory, showing that the mitochondria have lost their ability to maintain their membrane potential, a measure of mitochondrial fitness.
O’Malley is investigating whether the two genes linked to Parkinson’s disease affect mitochondria damaged by the toxin.
If you think, for example, of a peripheral nerve, the cell body is located in the spine, but some of the axons extend to the toe, says O’Malley, a professor neurobiology. It ‘s like the cell body is located in an office in St. Louis and the end of the axon is in Chicago.
For the study, O’Malley gave cultured mouse nerve cells a toxin called MPP +, which causes symptoms similar to Parkinson’s.
We will continue to look for specific differences in these cells that could help scientists develop better treatments, said O’Malley.
New research shows that a drug known to damage nerve cells that produce dopamine and mimic Parkinson’s disease is rapidly damage the cellular power generators called mitochondria. This damage impairs the ability of mitochondria to circulate around the cell as they would normally. As a result, axons, the nerve cells of the outstretched arm to use to send messages, wither, and a few days later, the body or main part of the cell dies.
Dopamine is involved in brain cell communication, including the signals that control movement. Parkinson’s disease kills cells that produce dopamine, patients begin to develop tremors, movement problems and other symptoms.
The new data offer advice as to why so many wrongs selectively brain cells that produce dopamine, say researchers at the University of Washington School of Medicine in St. Louis.
O’Malley found that the toxin stopped the movement of mitochondria in the axon in 30 minutes. The railroad was still in operation, the dispatch of goods to the other end of the axon. But most of the mitochondria stopped moving or is moving toward the cell body instead of the axon.
The specificity of this toxin for dopamine-producing cells is reinforced by the fact that other types of nerve cells do not have transportation problems of the mitochondria after exposure to toxins. In a comparison between different types of nerve cells, O’Malley found mitochondria in nerve cells that produce dopamine are smaller in size and travel three times slower.
But you can not say with certainty that these distinctions have a role in the problems caused by the toxin.