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BPS3011 Disease-focused pharmacology S1 2025

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Convince

a funding panel to support your schizophrenia research.

You are applying for a research

grant to develop a new therapeutic approach for schizophrenia.

In a short written pitch

,

persuade the panel that your project is worth funding by addressing the

following:

  • Why is schizophrenia a critical area for

    research investment?

  • What gap or limitation in current treatment

    does your project aim to address?

  • What potential impact could your research have

    on patients or healthcare?

Write your response as if you are

speaking to a panel of non-specialist reviewers—keep it clear, persuasive, and

focused on real-world relevance.

[10 marks, 10 minutes]

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Atypical antipsychotics are commonly

prescribed to manage schizophrenia.

Explain how these medications work and

why they may be more effective than typical antipsychotics for some patients.

[5 marks, 5 minutes]

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A patient newly diagnosed with

schizophrenia presents with predominantly negative and cognitive symptoms and

is concerned about side effects.

Which class of antipsychotic would you

recommend (typical vs. atypical), and why?

[5

marks, 5 minutes]

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You are a clinician explaining

Alzheimer’s disease progression to a patient’s family member.

Using plain language, describe what happens to the brain structurally and

chemically in AD and how this explains the patient’s:

  • Memory

    loss

  • Difficulty

    with speech or language

  • Confusion

    and personality changes

Your response should explain links between brain region damage (e.g.

hippocampus, cortex), cholinergic deficits, and hallmark pathology (plaques and

tangles).

[8 marks,

10 minutes]

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You are

part of a clinical trial team evaluating two experimental Alzheimer’s disease

treatments:

  • Drug A:

    A

    monoclonal antibody that targets amyloid-beta oligomers

  • Drug B:

    A

    small molecule that inhibits tau hyperphosphorylation

Critically

evaluate which drug is more likely to have a greater impact on improving

cognitive function in the early stages of Alzheimer’s disease.

In your answer:

  • Explain the role of amyloid-beta and tau in

    disease progression

  • Evaluate the likely effectiveness of targeting

    each in early-stage patients

  • Make and justify a recommendation on which

    should progress to Phase III trials

[8 marks, 10 minutes]

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You must read and agree to the academic declaration before you can access the quiz.

Academic integrity and honesty declaration

I am committed to upholding Monash University standards of academic integrity and honesty, and I agree to do the following in this non-invigilated online assessment:

  • I will complete this assessment individually, and will NOT participate in any unauthorised collaboration (collusion) when completing this assessment.
  • I will not plagiarise the work of others or include work that has been previously submitted as part of another unit/course (plagiarism).
  • I will take reasonable steps to safeguard my answers to the assessment and to ensure that other students are unable to copy or misuse my work.
  • I will follow all the requirements of Monash University's Student Academic Integrity Policy and Procedures.
  • I will be responsible for the consequences of engaging in plagiarism and collusion as described in Part 7 of the Monash University (Council) Regulations (academic misconduct)

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Explain the mechanism of action of memantine and indicate why it may be prescribed in Alzheimer’s disease; what is the physiological rationale for use?

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Describe the changes in the brain of a patient with Alzheimer’s disease, with regards to cholinergic transmission. Explain the mechanism of action of anticholinesterases and indicate why they may be prescribed in Alzheimer’s disease; what is their physiological rationale for use?

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Explain the role of cholinergic transmission in learning and memory.

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Explain the role of glutamatergic signalling in learning and memory. In your answer indicate the role of AMPA and NMDA receptors, and describe the resultant changes in synaptic plasticity. What physical changes within the dendrites of a neurone may occur to engender or promote longer-term changes in synaptic architecture?

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