Symptoms of Parkinsonandrsquo;s Disease, such as tremors, are thought to be caused by low dopamine levels in the brain.Current treatments of Parkinsonandrsquo;s disease are primarily reactionary, aiming to replenish dopamine levels after dopamine-producing neurons in the brain have died.Without a more detailed understanding of the behavior of dopamine-producing neurons, it has been impossible to develop treatments that would prevent the destruction of these neurons in Parkinsonandrsquo;s patients.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 alphasynuclein 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 Parkinsonandrsquo;s patients, but other causes may exist. Most scientists involved with Parkinsonandrsquo;s research do agree, however, that such promising early results provide a basis for further testing.Q.It can be inferred from the passage that current treatments of Parkinsonandrsquo;s Diseasea)repair damaged cells by replenishing dopamine levels in the brainb)are ineffective in their treatment of Parkinsonandrsquo;s symptoms, such as tremorsc)were developed without a complete understanding of dopamine-producing neuronsd)will inevitably be replaced by new drug therapy to suppress alpha-synuclein toxicitye)were not developed through research on yeast cellsCorrect answer is option 'C'. Can you explain this answer?

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Symptoms of Parkinson’s Disease, such as tremors, are thought to be caused by low dopamine levels in the brain.
Current treatments of Parkinson’s disease are primarily reactionary, aiming to replenish dopamine levels after dopamine-producing neurons in the brain have died.
Without a more detailed understanding of the behavior of dopamine-producing neurons, it has been impossible to develop treatments that would prevent the destruction of these neurons in Parkinson’s patients.
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 alphasynuclein 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.
Q.
It can be inferred from the passage that current treatments of Parkinson’s Disease

a)
repair damaged cells by replenishing dopamine levels in the brain
b)
are ineffective in their treatment of Parkinson’s symptoms, such as tremors
c)
were developed without a complete understanding of dopamine-producing neurons
d)
will inevitably be replaced by new drug therapy to suppress alpha-synuclein toxicity
e)
were not developed through research on yeast cells

Correct answer is option 'C'. Can you explain this answer?

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Symptoms of Parkinson’s Disease, such as tremors, are thought to...

his is a specific question. We can use the key phrase “current treatments of Parkinson’s Disease” from the question to help us locate the relevant portion of the passage. The first paragraph discusses current treatments.
(A) Current treatments do not repair damaged cells. Rather, they “are primarily reactionary, aiming to replenish dopamine levels after dopamine-producing neurons in the brain have died.”
(B) The passage does not discuss the effectiveness of current treatments.
(C) CORRECT. The first paragraph states that current treatments “replenish dopamine levels after dopamine-producing neurons in the brain have died.” It goes on to say that “without a more detailed understanding of the behavior of dopamineproducing neurons, it has been impossible to develop treatments that would prevent the destruction of these neurons in Parkinson’s patients.” We can therefore conclude that current treatments are based on an incomplete understanding of the dopamineproducing neuron.
(D) While the passage gives hope that new drug therapy will be effective, the fourth paragraph introduces the possibility that such treatments won’t be transferable to humans: “researchers are hesitant to conclude that such therapies will prove successful on human patients.” Thus, the claim that current treatments will inevitably be replaced by new drug therapy is unsupported by the passage.
(E) There is no information in the passage on the methods used to develop current treatments. It is very possible that yeast cells were used in researching current treatments.

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Symptoms of Parkinson’s Disease, such as tremors, are thought to be caused by low dopamine levels in the brain.Current treatments of Parkinson’s disease are primarily reactionary, aiming to replenish dopamine levels after dopamine-producing neurons in the brain have died.Without a more detailed understanding of the behavior of dopamine-producing neurons, it has been impossible to develop treatments that would prevent the destruction of these neurons in Parkinson’s patients.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 alphasynuclein 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.Q.It can be inferred from the passage that a yeast cell with toxic levels of alpha-synuclein will die because

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Symptoms of Parkinson’s Disease, such as tremors, are thought to be caused by low dopamine levels in the brain.Current treatments of Parkinson’s disease are primarily reactionary, aiming to replenish dopamine levels after dopamine-producing neurons in the brain have died.Without a more detailed understanding of the behavior of dopamine-producing neurons, it has been impossible to develop treatments that would prevent the destruction of these neurons in Parkinson’s patients.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 alphasynuclein 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.Q.One function of the third paragraph of the passage is to

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Symptoms of Parkinson’s Disease, such as tremors, are thought to be caused by low dopamine levels in the brain.Current treatments of Parkinson’s disease are primarily reactionary, aiming to replenish dopamine levels after dopamine-producing neurons in the brain have died.Without a more detailed understanding of the behavior of dopamine-producing neurons, it has been impossible to develop treatments that would prevent the destruction of these neurons in Parkinson’s patients.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 alphasynuclein 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.Q.According to the passage, which of the following represents the chronology of a typical protein life in a healthy yeast cell?

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One of the foundations of scientific research is that an experimental result is credible only if it can be replicated—only if performing the experiment a second time leads to the same result. But physicists John Sommerer and Edward Ott have conceived of a physical system in which even the least change in the starting conditions—no matter how small, inadvertent, or undetectable—can alter results radically. The system is represented by a computer model of a mathematical equation describing the motion of a particle placed in a particular type of force field.Sommerer and Ott based their system on an analogy with the phenomena known as riddled basins of attraction. If two bodies of water bound a large landmass and water is spilled somewhere on the land, the water will eventually make its way to one or the other body of water, its destination depending on such factors as where the water is spilled and the geographic features that shape the water’s path and velocity. The basin of attraction for a body of water is the area of land that, whenever water is spilled on it, always directs the spilled water to that body.In some geographical formations it is sometimes impossible to predict, not only the exact destination of the spilled water, but even which body of water it will end up in. This is because the boundary between one basin of attraction and another is riddled with fractal properties; in other words, the boundary is permeated by an extraordinarily high number of physical irregularities such as notches or zigzags. Along such a boundary, the only way to determine where spilled water will flow at any given point is actually to spill it and observe its motion; spilling the water at any immediately adjacent point could give the water an entirely different path, velocity, or destination.In the system posited by the two physicists, this boundary expands to include the whole system: i.e., the entire force field is riddled with fractal properties, and it is impossible to predict even the general destination of the particle given its starting point. Sommerer and Ott make a distinction between this type of uncertainty and that known as “chaos”; under chaos, a particle’s general destination would be predictable but its path and exact destination would not.There are presumably other such systems because the equation the physicists used to construct the computer model was literally the first one they attempted, and the likelihood that they chose the only equation that would lead to an unstable system is small. If other such systems do exist, metaphorical examples of riddled basins of attraction may abound in the failed attempts of scientists to replicate previous experimental results—in which case, scientists would be forced to question one of the basic principles that guide their work.According to the passage, Sommerer and Ott’s model differs from a riddled basin of attraction in which one of the following ways?

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One of the foundations of scientific research is that an experimental result is credible only if it can be replicated—only if performing the experiment a second time leads to the same result. But physicists John Sommerer and Edward Ott have conceived of a physical system in which even the least change in the starting conditions—no matter how small, inadvertent, or undetectable—can alter results radically. The system is represented by a computer model of a mathematical equation describing the motion of a particle placed in a particular type of force field.Sommerer and Ott based their system on an analogy with the phenomena known as riddled basins of attraction. If two bodies of water bound a large landmass and water is spilled somewhere on the land, the water will eventually make its way to one or the other body of water, its destination depending on such factors as where the water is spilled and the geographic features that shape the water’s path and velocity. The basin of attraction for a body of water is the area of land that, whenever water is spilled on it, always directs the spilled water to that body.In some geographical formations it is sometimes impossible to predict, not only the exact destination of the spilled water, but even which body of water it will end up in. This is because the boundary between one basin of attraction and another is riddled with fractal properties; in other words, the boundary is permeated by an extraordinarily high number of physical irregularities such as notches or zigzags. Along such a boundary, the only way to determine where spilled water will flow at any given point is actually to spill it and observe its motion; spilling the water at any immediately adjacent point could give the water an entirely different path, velocity, or destination.In the system posited by the two physicists, this boundary expands to include the whole system: i.e., the entire force field is riddled with fractal properties, and it is impossible to predict even the general destination of the particle given its starting point. Sommerer and Ott make a distinction between this type of uncertainty and that known as “chaos”; under chaos, a particle’s general destination would be predictable but its path and exact destination would not.There are presumably other such systems because the equation the physicists used to construct the computer model was literally the first one they attempted, and the likelihood that they chose the only equation that would lead to an unstable system is small. If other such systems do exist, metaphorical examples of riddled basins of attraction may abound in the failed attempts of scientists to replicate previous experimental results—in which case, scientists would be forced to question one of the basic principles that guide their work.Which one of the following most accurately expresses the main point of the passage?

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Symptoms of Parkinson’s Disease, such as tremors, are thought to be caused by low dopamine levels in the brain.Current treatments of Parkinson’s disease are primarily reactionary, aiming to replenish dopamine levels after dopamine-producing neurons in the brain have died.Without a more detailed understanding of the behavior of dopamine-producing neurons, it has been impossible to develop treatments that would prevent the destruction of these neurons in Parkinson’s patients.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 alphasynuclein 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.Q.It can be inferred from the passage that current treatments of Parkinson’s Diseasea)repair damaged cells by replenishing dopamine levels in the brainb)are ineffective in their treatment of Parkinson’s symptoms, such as tremorsc)were developed without a complete understanding of dopamine-producing neuronsd)will inevitably be replaced by new drug therapy to suppress alpha-synuclein toxicitye)were not developed through research on yeast cellsCorrect answer is option 'C'. Can you explain this answer?

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Symptoms of Parkinson’s Disease, such as tremors, are thought to be caused by low dopamine levels in the brain.Current treatments of Parkinson’s disease are primarily reactionary, aiming to replenish dopamine levels after dopamine-producing neurons in the brain have died.Without a more detailed understanding of the behavior of dopamine-producing neurons, it has been impossible to develop treatments that would prevent the destruction of these neurons in Parkinson’s patients.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 alphasynuclein 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.Q.It can be inferred from the passage that current treatments of Parkinson’s Diseasea)repair damaged cells by replenishing dopamine levels in the brainb)are ineffective in their treatment of Parkinson’s symptoms, such as tremorsc)were developed without a complete understanding of dopamine-producing neuronsd)will inevitably be replaced by new drug therapy to suppress alpha-synuclein toxicitye)were not developed through research on yeast cellsCorrect answer is option 'C'. Can you explain this answer? for GMAT 2024 is part of GMAT preparation. The Question and answers have been prepared according to the GMAT exam syllabus. Information about Symptoms of Parkinson’s Disease, such as tremors, are thought to be caused by low dopamine levels in the brain.Current treatments of Parkinson’s disease are primarily reactionary, aiming to replenish dopamine levels after dopamine-producing neurons in the brain have died.Without a more detailed understanding of the behavior of dopamine-producing neurons, it has been impossible to develop treatments that would prevent the destruction of these neurons in Parkinson’s patients.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 alphasynuclein 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.Q.It can be inferred from the passage that current treatments of Parkinson’s Diseasea)repair damaged cells by replenishing dopamine levels in the brainb)are ineffective in their treatment of Parkinson’s symptoms, such as tremorsc)were developed without a complete understanding of dopamine-producing neuronsd)will inevitably be replaced by new drug therapy to suppress alpha-synuclein toxicitye)were not developed through research on yeast cellsCorrect answer is option 'C'. Can you explain this answer? covers all topics & solutions for GMAT 2024 Exam. Find important definitions, questions, meanings, examples, exercises and tests below for Symptoms of Parkinson’s Disease, such as tremors, are thought to be caused by low dopamine levels in the brain.Current treatments of Parkinson’s disease are primarily reactionary, aiming to replenish dopamine levels after dopamine-producing neurons in the brain have died.Without a more detailed understanding of the behavior of dopamine-producing neurons, it has been impossible to develop treatments that would prevent the destruction of these neurons in Parkinson’s patients.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 alphasynuclein 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.Q.It can be inferred from the passage that current treatments of Parkinson’s Diseasea)repair damaged cells by replenishing dopamine levels in the brainb)are ineffective in their treatment of Parkinson’s symptoms, such as tremorsc)were developed without a complete understanding of dopamine-producing neuronsd)will inevitably be replaced by new drug therapy to suppress alpha-synuclein toxicitye)were not developed through research on yeast cellsCorrect answer is option 'C'. Can you explain this answer?.

Solutions for Symptoms of Parkinson’s Disease, such as tremors, are thought to be caused by low dopamine levels in the brain.Current treatments of Parkinson’s disease are primarily reactionary, aiming to replenish dopamine levels after dopamine-producing neurons in the brain have died.Without a more detailed understanding of the behavior of dopamine-producing neurons, it has been impossible to develop treatments that would prevent the destruction of these neurons in Parkinson’s patients.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 alphasynuclein 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.Q.It can be inferred from the passage that current treatments of Parkinson’s Diseasea)repair damaged cells by replenishing dopamine levels in the brainb)are ineffective in their treatment of Parkinson’s symptoms, such as tremorsc)were developed without a complete understanding of dopamine-producing neuronsd)will inevitably be replaced by new drug therapy to suppress alpha-synuclein toxicitye)were not developed through research on yeast cellsCorrect answer is option 'C'. Can you explain this answer? in English & in Hindi are available as part of our courses for GMAT. Download more important topics, notes, lectures and mock test series for GMAT Exam by signing up for free.

Here you can find the meaning of Symptoms of Parkinson’s Disease, such as tremors, are thought to be caused by low dopamine levels in the brain.Current treatments of Parkinson’s disease are primarily reactionary, aiming to replenish dopamine levels after dopamine-producing neurons in the brain have died.Without a more detailed understanding of the behavior of dopamine-producing neurons, it has been impossible to develop treatments that would prevent the destruction of these neurons in Parkinson’s patients.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 alphasynuclein 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.Q.It can be inferred from the passage that current treatments of Parkinson’s Diseasea)repair damaged cells by replenishing dopamine levels in the brainb)are ineffective in their treatment of Parkinson’s symptoms, such as tremorsc)were developed without a complete understanding of dopamine-producing neuronsd)will inevitably be replaced by new drug therapy to suppress alpha-synuclein toxicitye)were not developed through research on yeast cellsCorrect answer is option 'C'. Can you explain this answer? defined & explained in the simplest way possible. Besides giving the explanation of Symptoms of Parkinson’s Disease, such as tremors, are thought to be caused by low dopamine levels in the brain.Current treatments of Parkinson’s disease are primarily reactionary, aiming to replenish dopamine levels after dopamine-producing neurons in the brain have died.Without a more detailed understanding of the behavior of dopamine-producing neurons, it has been impossible to develop treatments that would prevent the destruction of these neurons in Parkinson’s patients.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 alphasynuclein 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.Q.It can be inferred from the passage that current treatments of Parkinson’s Diseasea)repair damaged cells by replenishing dopamine levels in the brainb)are ineffective in their treatment of Parkinson’s symptoms, such as tremorsc)were developed without a complete understanding of dopamine-producing neuronsd)will inevitably be replaced by new drug therapy to suppress alpha-synuclein toxicitye)were not developed through research on yeast cellsCorrect answer is option 'C'. Can you explain this answer?, a detailed solution for Symptoms of Parkinson’s Disease, such as tremors, are thought to be caused by low dopamine levels in the brain.Current treatments of Parkinson’s disease are primarily reactionary, aiming to replenish dopamine levels after dopamine-producing neurons in the brain have died.Without a more detailed understanding of the behavior of dopamine-producing neurons, it has been impossible to develop treatments that would prevent the destruction of these neurons in Parkinson’s patients.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 alphasynuclein 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.Q.It can be inferred from the passage that current treatments of Parkinson’s Diseasea)repair damaged cells by replenishing dopamine levels in the brainb)are ineffective in their treatment of Parkinson’s symptoms, such as tremorsc)were developed without a complete understanding of dopamine-producing neuronsd)will inevitably be replaced by new drug therapy to suppress alpha-synuclein toxicitye)were not developed through research on yeast cellsCorrect answer is option 'C'. Can you explain this answer? has been provided alongside types of Symptoms of Parkinson’s Disease, such as tremors, are thought to be caused by low dopamine levels in the brain.Current treatments of Parkinson’s disease are primarily reactionary, aiming to replenish dopamine levels after dopamine-producing neurons in the brain have died.Without a more detailed understanding of the behavior of dopamine-producing neurons, it has been impossible to develop treatments that would prevent the destruction of these neurons in Parkinson’s patients.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 alphasynuclein 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.Q.It can be inferred from the passage that current treatments of Parkinson’s Diseasea)repair damaged cells by replenishing dopamine levels in the brainb)are ineffective in their treatment of Parkinson’s symptoms, such as tremorsc)were developed without a complete understanding of dopamine-producing neuronsd)will inevitably be replaced by new drug therapy to suppress alpha-synuclein toxicitye)were not developed through research on yeast cellsCorrect answer is option 'C'. Can you explain this answer? theory, EduRev gives you an ample number of questions to practice Symptoms of Parkinson’s Disease, such as tremors, are thought to be caused by low dopamine levels in the brain.Current treatments of Parkinson’s disease are primarily reactionary, aiming to replenish dopamine levels after dopamine-producing neurons in the brain have died.Without a more detailed understanding of the behavior of dopamine-producing neurons, it has been impossible to develop treatments that would prevent the destruction of these neurons in Parkinson’s patients.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 alphasynuclein 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.Q.It can be inferred from the passage that current treatments of Parkinson’s Diseasea)repair damaged cells by replenishing dopamine levels in the brainb)are ineffective in their treatment of Parkinson’s symptoms, such as tremorsc)were developed without a complete understanding of dopamine-producing neuronsd)will inevitably be replaced by new drug therapy to suppress alpha-synuclein toxicitye)were not developed through research on yeast cellsCorrect answer is option 'C'. Can you explain this answer? tests, examples and also practice GMAT tests.

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