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BPS3011 Disease-focused pharmacology S1 2025

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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]

View this question

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]

View this question

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]

View this question

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]

View this question

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]

View this question

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]

View this question

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]

View this question

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]

View this question

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]

View this question

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