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BPS3011 Disease-focused pharmacology S1 2025

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You are a researcher working on Schizophrenia disease (in 2025). You are submitting your first grant application and now need to draft a convincing opening paragraph that indicates the significance and need for your research to be funded. What information or supporting data would you include? Outline your project overview, the gaps or challenges you are addressing and the rationale for embarking on this program of research (ballpark, 250 words).

Feel free to use the structure below to guide your paragraph:

  • Have you conveyed the impact on the community? Is epidemiology data included to set the scene?
  • Have you articulated how the disease is currently treated?
  • Have you described what the current gaps are?

  • Have you discussed what the project will aim to do?

[10 marks, 10 minutes]

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Anna is a 28-year-old woman who has been experiencing unusual thoughts and paranoid beliefs for the past few weeks. Her family members are concerned and take her to a healthcare provider and over the next 6 month, she is diagnosed with schizophrenia. The healthcare provider prescribes her an antipsychotic medication.

Anna's family members ask about the effectiveness of current antipsychotic medications. What would you tell them?

Anna's family members then ask about the side effects of the medication. What would you tell them?

Finally, Anna's family members ask about the long-term effectiveness of the medication. What would you tell them?

[5 marks, 5 minutes]

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Schizophrenia is associated with positive, negative and cognitive symptoms. Define each domain of symptoms including at least one specific example of how each might manifest in an individual and the underlying pathophysiology thought to be involved in each domain of symptoms.

Pharmacotherapies exist to treat the positive and negative symptom domains of schizophrenia however there is still a need to advance novel drug treatments for Schizophrenia. Discuss TWO major contributors (covered during class discussion) that might impede the progress of a future drug candidate for the treatment of schizophrenia in the area of neuroscience drug discovery.

[8 marks, 10 minutes]

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Patients with Alzheimer’s disease are prescribed memantine (NMDA receptor antagonist). Using accessible language, explain how this medication works, and why you might describe the mechanism using the Goldilocks analogy – i.e. ‘not too much or not too little, but just right’. Address what the consequences would be if there was 'too much or too little'.

[5 marks, 5 minutes]

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Use lay / simple language to describe 4-5 different symptoms of Alzheimer’s disease. Explain what normal processes are disrupted in Alzheimer’s disease, and how this pathophysiology results in the symptoms observed.

Now, use pen and paper or digital drawing to create a two-panel image that illustrates the neuronal changes that underpin learning and memory, and then the consequences of the Alzheimer’s disease pathology on cognition. Consider the role of amyloid-beta and tau proteins in the pathophysiology of Alzheimer's disease. How do abnormalities in these proteins contribute to the development of AD, and what impact do these disruptions have on function and cognition?

[8 marks, 10 minutes]

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Why is

developing drugs for central nervous system (CNS) disorders like schizophrenia

particularly challenging?

In your response, consider:

  • Biological and diagnostic complexity
  • Limitations of current animal models
  • Side effect profiles
  • Translational gaps between pre-clinical and

    clinical phases

[5 marks,

5 minutes]

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The dopamine hypothesis and

glutamate hypothesis are two major models explaining the neurochemical basis of

schizophrenia.

Critically

compare these two hypotheses,

including:

  • The key neurochemical changes proposed in each
  • The types of symptoms each hypothesis explains

    (positive, negative, cognitive)

  • How current and emerging treatments align with

    these models

  • Which hypothesis you think offers a better

    framework for future drug discovery, and why

[8 marks, 8 minutes]

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Researchers are investigating the

effects of a tau aggregation inhibitor on synaptic structure and function in a

mouse model of Alzheimer’s disease. You are given the following experimental

data:

Group

Spine

Density (spines/μm)

 

Synaptic

Plasticity (LTP%)

Cognitive

Performance (Maze Test Time)

Healthy

Control (n=12)

1.2

150%

40 sec

Untreated

AD Model (n=11)

0.5

85%

120 sec

AD

+ Tau Inhibitor Drug (n=13)

1.0

135%

55 sec

 

Task:

Using the data above and your

understanding of Alzheimer’s disease pathophysiology,

write a response that

explains

:

  1. The role of tau protein in healthy neurons

    ,

    and how

    tau pathology

    affects dendritic structure and synaptic

    plasticity in Alzheimer’s disease

  2. How the tau aggregation inhibitor

    appears to be changing synaptic structure and function in all the groups,

    based on the experimental data

  3. How these cellular-level changes correlate

    with the observed differences in

    maze performance between groups

[10

marks, 10 minutes]

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Critically evaluate a new drug

that targets tau aggregation.

This hypothetical drug prevents the formation of neurofibrillary tangles by

stabilising tau proteins. As a student-researcher:

  • Describe

    how this drug might alter disease progression

  • Identify

    potential benefits and limitations

  • Propose

    an experiment to test its efficacy in a pre-clinical model

  • Explain

    how this could address current gaps in AD therapy

[8 marks,

8 minutes]

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Rivastigmine

is commonly prescribed for patients with Alzheimer’s disease.

Explain how this drug

works and why it may improve symptoms in people with Alzheimer’s disease.

In your answer, refer to acetylcholine and the brain changes seen in AD.

[

5

marks]

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