Symptoms of Parkinson’s Disease, such as tremors, are thought to be caused by low dopamine levels in the brain. Current
Recent research provides insight into the inner workings of dopamine-producing neurons, and may lead to a new drug treatment that would proactively protect the neurons from decay. By examining the alpha-synuclein protein in yeast cells, scientists have determined that toxic levels of the protein have a detrimental effect on protein transfer within the cell. More specifically, high levels of alpha-synuclein disrupt the flow of proteins from the endoplasmic reticulum, the site of protein production in the cell, to the Golgi apparatus, the component of the cell that modifies and sorts the proteins before sending them to their final destinations within the cell. When the smooth transfer of proteins from the endoplasmic reticulum to the Golgi apparatus is interrupted, the cell dies.
With this in mind, researchers conducted a genetic screen in yeast cells in order to identify any gene that works to reverse the toxic levels of alpha-synuclein in the cell. Researchers discovered that such a gene does in fact exist, and have located the genetic counterpart in mammalian nerve cells, or neurons. This discovery has led to new hopes that drug therapy could potentially activate this gene, thereby suppressing the toxicity of alpha-synuclein in dopamine-producing neurons.
While drug therapy to suppress alpha-synuclein has been examined in yeast, fruitflies, roundworms, and cultures of rat neurons, researchers are hesitant to conclude that such therapies will prove successful on human patients. Alpha-synuclein toxicity seems to be one cause for the death of dopamine-producing neurons in Parkinson’s patients, but other causes may exist. Most scientists involved with Parkinson’s research do agree, however, that such promising early results provide a basis for further testing.
Which of the following statements regarding a high level of
AIt is not a cause for the death of neurons in Parkinson’s patients, though it has led to other research that may prove fruitful.
BIts effect on human neurons cannot be tested.
CIt is one possible cause for the death of neurons in Parkinson’s patients, but not the only one.
DIts detrimental effect on human neurons can be prevented through drug therapy.
EIt is the only possible cause for the death of neurons in Parkinson’s patients.
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