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29 Aug 2018

We covered the neuroscience, cognitive behavioral and genetic paradigms in this module. Please rank them based on their ability to explain psychological disorder. Then briefly explain your ranking in less than a paragraph. For example you could rank 1) neuroscience 2) cognitive behavioral and 3) genetic paradigms and speak about how the increase in psychotropic medications may mean they are working.

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Beverley SmithLv2

1 Sep 2018

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Related questions

Physiology Psychology

1. The mind-body problem is a fundamental philosophical issue at the base of all cognitive/behavioral neuroscience research. Why? Discuss the mind-body problem and give an example of how it relates to an issue in cognitive/behavioral neuroscience. Explain.

2. Explain how an action potential occurs. Start with Glutamate release from the presynaptic neuron and end with neurotransmitter release from the postsynaptic neuron.

3. How does a neuron inhibit another neuron? Explain. {~1 paragraph}

4. Design a drug that would increase Dopamine (DA) and/or Norepinephrine (NE) levels and explain its mechanism of action (explain how it works to increase DA and/or NE). What kind of disorder could this drug be used to treat? What would be some side-effects you might expect from taking such a drug? Would there be any risks expected from long-term treatment? Explain.

5. Alzheimerâs dementia is a neurodegenerative disorder that results in severe cognitive impairment. Researchers hypothesize that Alzheimerâs is due to low Acetylcholine activity in the cerebral cortex. How could a researcher test this hypothesis? Justify your answer.

6. What is neural plasticity? Give an example and explain. [3-4 sentences]

7. Dr. Butthurt, a prominent pain researcher, has recently discovered that a Chinese form of meditation called Tai Chi can be a very effective pain-relief method. In Dr. Butthurtâs studies, he found that people in pain experience profound pain relief after participating in just 30 minutes of Tai Chi meditation. Now, Dr. Butthurt wants to determine the neural mechanism by which Tai Chi works to relieve pain. The first hypothesis he wants to test is that Tai Chi works because it stimulates endorphin activity in the brain. How can Dr. Butt-hurt test this hypothesis? Explain. [~1 paragraph]

8. A dominant view in neuroscience is that the human brain is âmodularâ. For example, many have claimed that the Fusiform Face Area (FFA) is a specialized, domain-specific module for recognizing faces. Discuss the issue, giving evidence for and against the claim that the FFA is domain-specific for face-processing. (1-2 paragraphs)

9. The Wernicke-Geschwind model of language was the dogma in neuroscience and psychology for many years. According to the W-G model, Brocaâs Area and Wernickeâs area are the two main language modules in the brain. What does the model argue is the function of Brocaâs area? Explain one piece of evidence to support it. What does the model argue is the function of Wernickeâs area? Explain one piece of evidence to support it. Why has the current theory of language moved away from the W-G Model? Explain.

10. If a person has the genes associated with a particular psychopathological disorder (e.g., depression, schizophrenia, bipolar, etc), will that person definitely develop the disorder? Why or why not? Explain. Use an example to help you explain. (few sentences to a short paragraph)

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12. How does Miraculin act on the nervous system to change our perception of taste? Explain.

13. Discuss the Triune Brain model. Explain what happens to the functioning of the Triune Brain model when an individual is intoxicated by alcohol, and link that to drunk behavior.

14. Some patients develop disorders in which they believe that one of their limbs is not, in fact, their own limb. What could be happening in the nervous system that would lead to this peculiar phenomenon? Justify your answer and explain. (I am looking for you to come up with a reasonable hypothesis as to what could be causing it that you can sensibly justify and explain)

15a. What is schizophrenia? Describe 2 positive and 2 negative symptoms. Explain one way that the brains of schizophrenic patients are different from healthy controls, and link the brain abnormality to one of the symptoms of schizophrenia that you just described. 15b. What is the Dopamine (DA) Hypothesis for schizophrenia? Explain two pieces of evidence to support the DA Hypothesis. Explain one piece of evidence against the DA hypothesis. [~1 short paragraph] 15c. What is the Glutamate Hypothesis for schizophrenia? Explain two pieces of evidence to support the Glutamate hypothesis. Explain one piece of evidence against the Glutamate hypothesis. [~ 1 short paragraph] 15d. Schizophrenia is estimated to be about 80% heritable, but there are other factors that researchers have found to influence the development (or flare) of schizophrenia. Give an example of one of these other factors, and briefly explain the evidence for it. [2-3 sentences]

16. Major depression (unipolar) is a psychiatric disorder affecting over 15% of the U.S. population. Explain two of the dominant hypotheses about the biological factors in depression, discussing the evidence for and against those hypotheses. What is the most effective treatment for long-term relief from depression? Why? Explain. (~2 paragraphs)

17. Explain how the amygdala and brain stem are involved in the development of anxiety disorders such as PTSD, phobias or panic disorder.

18. Explain the basic function of the mesolimbic DA reward pathway. Discuss how drug use alters the pathway and contributes to the development of compulsive disorders like drug addictions/alcoholism.

19. If a stroke patient has damage to their right posterior parietal lobe, along the dorsal stream of visual processing, what syndrome would the patient have? Describe the major symptoms and explain what the personâs behavior would be like. What did we learn about the function of the parietal lobe from studying these patients? Explain.

20. If a stroke patient has damage to their temporal lobe, along the ventral stream of visual processing, what type of disorder would the patient have? Describe the major symptoms and explain what the personâs behavior would be like. What did we learn about the function of the temporal lobe from studying these patients? Explain.

21. What is blindsight? Explain how studying patients with blindsight informed our understanding of the visual system.

22. What are implicit and explicit memories? Do implicit and explicit memories represent independent neural systems for memory? Why or why not? Justify your answer with evidence.

23. What is retrograde amnesia? What did we learn about long-term memory from studying patients with retrograde amnesia (e.g., patient KC)? Explain.

24. What is our current understanding of how the Medial Temporal Lobe (MTL) stores and retrieves explicit memories? Discuss how the function of the MTL can explain cases of anterograde amnesia like HMâs.

25. Imagine that a doctor developed a drug called Memoryhole that is a Glutamate-NMDA receptor antagonist in the hippocampus. What effect would Memoryhole have on the process of Long-Term Potentiation (LTP), and, in turn, memory? Explain.

26. Do we have evidence for a biological basis for sexual preference? Discuss with respect to the Sexually Dimorphic Nucleus of the hypothalamus.

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28. Parkinsonâs disease is a neurodegenerative disorder that results in severe motor impairments. What causes Parkinsonâs? Explain the major treatment for the disorder and the extent to which the treatment is successful. Are there any negative side-effects of that treatment? Explain.

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30. What was the most interesting thing you learned in class this semester? Why did you find it interesting? Explain.

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Please answer the question after reading the paragraph.

We have a global health challenge in our hands today, and that is that the way we currently discover and develop new drugs is too costly, takes far too long, and it fails more often than it succeeds. It really just isn't working, and that means that patients that badly need new therapies are not getting them, and diseases are going untreated. We seem to be spending more and more money. So for every billion dollars we spend in R&D, we're getting less drugs approved into the market. More money, less drugs. Now we have a whole pipeline of different organ chips that we are currently working on in our labs. Now, the true power of this technology, however, really comes from the fact that we can fluidically link them. There's fluid flowing across these cells, so we can begin to interconnect multiple different chips together to form what we call a virtual human on a chip. Now we're really getting excited.We're not going to ever recreate a whole human in these chips, but what our goal is is to be able to recreate sufficient functionality so that we can make better predictions of what's going to happen in humans. For example, now we can begin to explore what happens when we put a drug like an aerosol drug. Those of you like me who have asthma, when you take your inhaler, we can explore how that drug comes into your lungs, how it enters the body, how it might affect, say, your heart. Does it change the beating of your heart? Does it have a toxicity? Does it get cleared by the liver? Is it metabolized in the liver? Is it excreted in your kidneys? We can begin to study the dynamic response of the body to a drug. Organs on chips could also change the way we do clinical trials in the future. Right now, the average participant in a clinical trial is that: average. Tends to be middle aged, tends to be female. You won't find many clinical trials in which children are involved, yet every day, we give children medications, and the only safety data we have on that drug is one that we obtained from adults. Children are not adults. They may not respond in the same way adults do. There are other things like genetic differences in populations that may lead to at-risk populations that are at risk of having an adverse drug reaction. Now imagine if we could take cells from all those different populations, put them on chips, and create populations on a chip. This could really change the way we do clinical trials. And this is the team and the people that are doing this. We have engineers, we have cell biologists, we have clinicians, all working together. We're really seeing something quite incredible at the Wyss Institute. It's really a convergence of disciplines, where biology is influencing the way we design, the way we engineer, the way we build. It's pretty exciting.

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If you are able to answer any or all of these that would begreat!!!

25. Talked about the warburg effect ( aerobic glycolysis) inwhich cancer cells preferentially use fermentation instead of goingthrough oxidative phosphorylation. Answer the followingquestions?

A) If cells are going to preferentially use fermentation, theyneed to transport higher levels of glucose into the cell. Explainwhy this is so?

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G What is a prediction that you could make based on yourhypothesis?

H) In the paper, the authors conclude that adding the PTEN backinto the cancer cells via transfection decreases the amount ofglucose that FTC133 cells take up. You hypothesize that HeLa cellsmight benefit from having additional PTEN protein. YOu transfectDNA coding for the PTEN protein into the HeLa cells and perform awestern blot to confirm PTEN expression. Unfortunately, you do notsee any expression of PTEN. What is one possible reason you dontget PTEN expression in your HeLa cells? ( HINT: you know yourantibodies are working and that transfection was successful, sothink about factors controlling gene expression)

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J) Next, you decide that you want to purify large amounts ofyour wild type and mutant PTEN proteins to test their catalyticabilities in in vitro. Your labmate suggests that you transform (insert) your DNA into bacterial cells because they are rapidlygrowing and are know to express large amounts of protein under theright conditions. You consider this but are unsure as to how wellyour human PTEN protein might be expressed in these cells. Based onwhat you know about the genetic code and about gene expression inprokaryotic and eukaryotic cells describe (i) one reason why yourgene might be able to be expressed in bacterial cells under theright conditions and (ii) two reasons why your PTEN gene might notbe expressed properly. (iii) Then, decribe one modification thatcould be made to your PTEN DNA to increase the likelihood that itwill be expresssed in the bacteria.