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 a yeast cell with toxic levels of alpha-synuclein will die becausea)low levels of dopamine will disrupt the flow of proteins from the endoplasmic reticulum to the Golgi apparatusb)the gene that suppresses alpha-synuclein is missing or is not functioning properly in such yeast cellsc)drug therapy has proven to be ineffective in yeast cellsd)the normal distribution of proteins to the different cell components outside the Golgi apparatus will be affectede)alpha-synuclein is by nature a toxic proteinCorrect answer is option 'D'. 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 a yeast cell with toxic levels of alpha-synuclein will die because

a)
low levels of dopamine will disrupt the flow of proteins from the endoplasmic reticulum to the Golgi apparatus
b)
the gene that suppresses alpha-synuclein is missing or is not functioning properly in such yeast cells
c)
drug therapy has proven to be ineffective in yeast cells
d)
the normal distribution of proteins to the different cell components outside the Golgi apparatus will be affected
e)
alpha-synuclein is by nature a toxic protein

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

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

This is a specific question that can be answered by examining the information given in the second paragraph.
(A) According the second paragraph, “high levels of alpha-synuclein disrupt the flow of proteins from the endoplasmic reticulum…to the Golgi apparatus,” not low levels of dopamine.
(B) While a missing or malfunctioning gene may explain why levels of alphasynuclein have risen to toxic levels in the cell, it does not explain why these high levels cause the cell to die.
(C) The effectiveness or ineffectiveness of drug therapy in yeast cells does not explain why high levels of alpha-synuclein would kill the cell. Furthermore, the fourth paragraph suggests that drug therapy actually has been effective in yeast cells, not to mention in fruitflies, roundworms, and cultures of rat neurons.
(D) CORRECT. The second paragraph states that high levels of alpha-synuclein “disrupt the flow of proteins from the endoplasmic reticulum…to the Golgi apparatus.” According to the passage, the Golgi apparatus is responsible for distributing proteins within the cell. It also states that "when the smooth transfer of proteins from the endoplasmic reticulum to the Golgi apparatus is interrupted, the cell dies."
(E) The passage gives no indication that alpha-synuclein is “by nature” a toxic substance. Rather, the passage states that high levels of alpha-synuclein are toxic to the cell.

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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

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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.Given the information in the passage, Sommerer and Ott are most likely to agree with which one of the following?

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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 becausea)low levels of dopamine will disrupt the flow of proteins from the endoplasmic reticulum to the Golgi apparatusb)the gene that suppresses alpha-synuclein is missing or is not functioning properly in such yeast cellsc)drug therapy has proven to be ineffective in yeast cellsd)the normal distribution of proteins to the different cell components outside the Golgi apparatus will be affectede)alpha-synuclein is by nature a toxic proteinCorrect answer is option 'D'. 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 a yeast cell with toxic levels of alpha-synuclein will die becausea)low levels of dopamine will disrupt the flow of proteins from the endoplasmic reticulum to the Golgi apparatusb)the gene that suppresses alpha-synuclein is missing or is not functioning properly in such yeast cellsc)drug therapy has proven to be ineffective in yeast cellsd)the normal distribution of proteins to the different cell components outside the Golgi apparatus will be affectede)alpha-synuclein is by nature a toxic proteinCorrect answer is option 'D'. 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 a yeast cell with toxic levels of alpha-synuclein will die becausea)low levels of dopamine will disrupt the flow of proteins from the endoplasmic reticulum to the Golgi apparatusb)the gene that suppresses alpha-synuclein is missing or is not functioning properly in such yeast cellsc)drug therapy has proven to be ineffective in yeast cellsd)the normal distribution of proteins to the different cell components outside the Golgi apparatus will be affectede)alpha-synuclein is by nature a toxic proteinCorrect answer is option 'D'. 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 a yeast cell with toxic levels of alpha-synuclein will die becausea)low levels of dopamine will disrupt the flow of proteins from the endoplasmic reticulum to the Golgi apparatusb)the gene that suppresses alpha-synuclein is missing or is not functioning properly in such yeast cellsc)drug therapy has proven to be ineffective in yeast cellsd)the normal distribution of proteins to the different cell components outside the Golgi apparatus will be affectede)alpha-synuclein is by nature a toxic proteinCorrect answer is option 'D'. 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 a yeast cell with toxic levels of alpha-synuclein will die becausea)low levels of dopamine will disrupt the flow of proteins from the endoplasmic reticulum to the Golgi apparatusb)the gene that suppresses alpha-synuclein is missing or is not functioning properly in such yeast cellsc)drug therapy has proven to be ineffective in yeast cellsd)the normal distribution of proteins to the different cell components outside the Golgi apparatus will be affectede)alpha-synuclein is by nature a toxic proteinCorrect answer is option 'D'. 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 a yeast cell with toxic levels of alpha-synuclein will die becausea)low levels of dopamine will disrupt the flow of proteins from the endoplasmic reticulum to the Golgi apparatusb)the gene that suppresses alpha-synuclein is missing or is not functioning properly in such yeast cellsc)drug therapy has proven to be ineffective in yeast cellsd)the normal distribution of proteins to the different cell components outside the Golgi apparatus will be affectede)alpha-synuclein is by nature a toxic proteinCorrect answer is option 'D'. 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 a yeast cell with toxic levels of alpha-synuclein will die becausea)low levels of dopamine will disrupt the flow of proteins from the endoplasmic reticulum to the Golgi apparatusb)the gene that suppresses alpha-synuclein is missing or is not functioning properly in such yeast cellsc)drug therapy has proven to be ineffective in yeast cellsd)the normal distribution of proteins to the different cell components outside the Golgi apparatus will be affectede)alpha-synuclein is by nature a toxic proteinCorrect answer is option 'D'. 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 a yeast cell with toxic levels of alpha-synuclein will die becausea)low levels of dopamine will disrupt the flow of proteins from the endoplasmic reticulum to the Golgi apparatusb)the gene that suppresses alpha-synuclein is missing or is not functioning properly in such yeast cellsc)drug therapy has proven to be ineffective in yeast cellsd)the normal distribution of proteins to the different cell components outside the Golgi apparatus will be affectede)alpha-synuclein is by nature a toxic proteinCorrect answer is option 'D'. 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 a yeast cell with toxic levels of alpha-synuclein will die becausea)low levels of dopamine will disrupt the flow of proteins from the endoplasmic reticulum to the Golgi apparatusb)the gene that suppresses alpha-synuclein is missing or is not functioning properly in such yeast cellsc)drug therapy has proven to be ineffective in yeast cellsd)the normal distribution of proteins to the different cell components outside the Golgi apparatus will be affectede)alpha-synuclein is by nature a toxic proteinCorrect answer is option 'D'. 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 a yeast cell with toxic levels of alpha-synuclein will die becausea)low levels of dopamine will disrupt the flow of proteins from the endoplasmic reticulum to the Golgi apparatusb)the gene that suppresses alpha-synuclein is missing or is not functioning properly in such yeast cellsc)drug therapy has proven to be ineffective in yeast cellsd)the normal distribution of proteins to the different cell components outside the Golgi apparatus will be affectede)alpha-synuclein is by nature a toxic proteinCorrect answer is option 'D'. Can you explain this answer? tests, examples and also practice GMAT tests.

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