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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 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]
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
,
and how
tau pathologyaffects dendritic structure and synaptic
plasticity in Alzheimer’s disease
appears to be changing synaptic structure and function in all the groups,
based on the experimental data
How these cellular-level changes correlate
with the observed differences in
maze performance between groups[10 marks, 10 minutes]
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]
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]
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]
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]
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]
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]
You are part of a clinical trial team evaluating two experimental Alzheimer’s disease treatments:
A
monoclonal antibody that targets amyloid-beta oligomers
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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