IB-psychology topic 1

Topic Title: Introduction to the Biological Approach

SUBTOPIC 1: Localization of Brain Function

Key Concepts and Definitions

Localization: The idea that different brain areas perform different functions.
Lateralization: Specialization of function in one hemisphere (e.g., language in the left).
Cortex: The outer layer responsible for higher-order processes like thought and decision-making.
Hippocampus: Involved in memory formation and spatial navigation.
Amygdala: Processes emotions such as fear.

Examples

Broca (1861): Patient “Tan” – left frontal damage impaired speech → Broca’s area.
Wernicke (1874): Damage to left posterior temporal area impaired comprehension.
Gazzaniga & Sperry (1968): Split-brain patients showed left hemisphere = language, right = spatial processing.
Maguire et al. (2000): London taxi drivers had larger posterior hippocampi → supports spatial memory localization.

SUBTOPIC 2: Techniques Used to Study the Brain

Key Concepts and Definitions

Brain imaging techniques: Allow investigation of the relationship between brain structure, activity, and behaviour.
Structural scans (e.g., MRI, CT): Show brain anatomy.
Functional scans (e.g., fMRI, PET, EEG): Show brain activity.

Core Terms

MRI (Magnetic Resonance Imaging): Provides detailed structural images.
fMRI (Functional MRI): Detects changes in blood flow indicating activity.
PET (Positron Emission Tomography): Measures metabolic activity using radioactive tracers.
EEG (Electroencephalogram): Measures electrical activity in the brain.

Examples

Maguire et al. (2000): MRI used to compare hippocampal volume in taxi drivers.
Antonova et al. (2011): fMRI used to examine acetylcholine’s effect on spatial memory.
Draganski et al. (2004): MRI scans before and after learning juggling to observe neuroplasticity.

SUBTOPIC 3: Neuroplasticity

Key Concepts and Definitions

Neuroplasticity: The brain’s ability to change structure and function in response to experience or damage.
Synaptic plasticity: Strengthening or weakening of synaptic connections.
Dendritic branching: Growth of dendritic connections from repeated stimulation.
Neural pruning: Elimination of unused connections.

Examples

Maguire et al. (2000): Taxi drivers’ hippocampus enlarged due to environmental demands.
Draganski et al. (2004): Juggling increased grey matter volume in visual and motor areas.
Rosenzweig & Bennett (1972): Rats in enriched environments developed thicker cortexes.

SUBTOPIC 4: Neurotransmission

Key Concepts and Definitions

Neurotransmission: Process by which neurons communicate through synapses.
Excitatory neurotransmitters: Increase likelihood of firing (e.g., dopamine).
Inhibitory neurotransmitters: Decrease likelihood of firing (e.g., GABA).

Examples

Antonova et al. (2011): Blocking acetylcholine impaired spatial memory.
Crockett et al. (2010): Serotonin increased prosocial behaviour in moral dilemmas.
Fisher, Aron & Brown (2005): Dopamine activity associated with romantic love.

SUBTOPIC 5: Hormones and Behaviour

Key Concepts and Definitions

Hormone: Chemical messenger secreted by glands into bloodstream influencing physiology and behaviour.
Endocrine system: Network of glands producing hormones.

Examples

Newcomer et al. (1999): Cortisol impaired verbal memory.
Ronay & von Hippel (2010): Testosterone increased risk-taking.
Scheele et al. (2012): Oxytocin increased monogamous behaviour in men.

SUBTOPIC 6: Pheromones and Behaviour

Key Concepts and Definitions

Pheromones: Chemical signals released by individuals that influence behaviour of others.

Core Terms

MHC (Major Histocompatibility Complex): Set of genes influencing immune system and mate preference.

Examples

Wedekind et al. (1995): Women preferred scent of men with dissimilar MHC → evolutionary advantage.

SUBTOPIC 7: Genetics and Behaviour

Key Concepts and Definitions

Genetics: Study of inheritance and gene expression in behaviour.
Heritability: Proportion of behaviour variation explained by genetics.
Epigenetics: How the environment can modify gene expression.

Core Terms

Monozygotic twins (MZ): Share 100% of genes.
Dizygotic twins (DZ): Share ~50% of genes.
Concordance rate: Likelihood both twins share a trait.

Examples

Kendler et al. (2006): Twin study found moderate heritability of depression.
Caspi et al. (2003): Interaction of 5-HTT gene with stressful events predicted depression.
Weaver et al. (2004): Maternal care altered stress gene expression in rats.

SUBTOPIC 8: Evolutionary Explanations of Behaviour

Key Concepts and Definitions

Natural selection: Traits increasing reproductive success become more common.
Adaptation: Behavioural changes improving survival.
Evolutionary psychology: Links evolutionary mechanisms to human behaviour.

Examples

Wedekind et al. (1995): Mate selection preferences reflect genetic diversity advantage.
Buss (1989): Cross-cultural study on mate preferences reflecting reproductive success factors.

SUBTOPIC 9: Animal Models in Biological Research

Key Concepts and Definitions

Animal models: Use of non-human species to study biological mechanisms of behaviour.

Examples

Ferguson et al. (2000): Oxytocin knockout mice lacked social recognition.
Weaver et al. (2004): Rat maternal care influenced stress response via epigenetics.
Rosenzweig & Bennett (1972): Environmental enrichment and cortical thickness.

Examiner Tips
🧠Localisation studies can be used as counter evidence for neuroplasticity responses and vice-versa to strengthen the argument
🧠Neuroplasticity studies on animals can double as studies for animal research topics
🧠Choose hormones that are also neurotransmitters, to be able to use overarching studies
🧠Some studies on pheromones can also be used for evolutionary psychology such as MHC genes
🧠Find studies that use brain imaging techniques, animal research, or have ethical concerns so that separate studies are not required for those topics.

* All studies suggested in the mark scheme are just examples, any studies that can be linked to the topics can be used.

Multiple Choice Questions

What does the term “localization” refer to in psychology?

a) The connection between synapses
b) Specific brain areas responsible for certain functions
c) The division between brain hemispheres
d) The process of neuroplasticity

Which part of the brain is primarily associated with higher-order functions like thought and creativity?
a) Cerebellum
b) Limbic system
c) Cortex
d) Brain stem
Dendritic branching is associated with which concept?
a) Neurotransmission
b) Neural pruning
c) Synaptic formation
d) Localization
Which brain lobe is responsible for processing visual input?
a) Frontal
b) Parietal
c) Occipital
d) Temporal
Which structure is part of the limbic system?
a) Cortex
b) Hippocampus
c) Cerebellum
d) Corpus Callosum
What was the aim of Maguire et al. (2000)?
a) Examine neuroplasticity and learning
b) Investigate spatial memory’s impact on hippocampal structure
c) Analyze neurotransmitters’ effect on mood
d) Assess brain function using EEG
What scanning technique did Maguire et al. use?
a) EEG
b) PET
c) MRI
d) CT
In Gazzaniga & Sperry’s split-brain study, what was a main finding?
a) Both hemispheres manage emotion
b) Language is right-hemisphere dominant
c) Corpus callosum integrates cognition
d) Spatial tasks handled by left hemisphere
What is neuroplasticity?
a) Fixed brain structure
b) Brain’s ability to change and adapt
c) A type of neurotransmitter
d) Genetic predisposition
Which neurotransmitter regulates mood and sleep?
a) Dopamine
b) Serotonin
c) GABA
d) ACh
What is the role of the amygdala?
a) Homeostasis
b) Visual processing
c) Fear response
d) Hunger regulation
Which imaging technique detects blood flow to show activity?
a) MRI
b) EEG
c) fMRI
d) CT
In Antonova et al., what did scopolamine do?
a) Increased spatial awareness
b) Lowered spatial awareness
c) No effect
d) Improved recall
Which hormone is known as the stress hormone?
a) Oxytocin
b) Melatonin
c) Cortisol
d) Adrenaline
Long-term potentiation (LTP) leads to:
a) Weaker signal
b) Stronger signal
c) Synaptic elimination
d) Neurogenesis
Which hormone is linked to bonding?
a) Cortisol
b) Oxytocin
c) Testosterone
d) Norepinephrine
What does EEG measure?
a) Brain chemicals
b) Electrical activity
c) Blood flow
d) Structural density
Which neurotransmitter calms the nervous system?
a) Serotonin
b) Dopamine
c) GABA
d) ACh
Wedekind et al. studied pheromones in relation to:
a) Visual memory
b) Mating behaviour
c) Long-term recall
d) Stress
Brain’s ability to eliminate unused connections is called:
a) Neural pruning
b) Dendritic branching
c) Synaptic plasticity
d) Neurogenesis
One criticism of evolutionary explanations is that they are:
a) Historically unsupported
b) Speculative and hard to test
c) Underestimate genetics
d) Ignore differences
Draganski et al. showed brain adaptability in the:
a) Temporal lobe
b) Frontal lobe
c) Parietal lobe
d) Mid-temporal lobe
Which study is the “smelly T-shirt” study?
a) Maguire
b) Gazzaniga
c) Draganski
d) Wedekind
Testosterone’s main behavioural effect is:
a) Maternal bonding
b) Memory retention
c) Risk-taking
d) Vision
Epigenetics refers to:
a) Fixed expression
b) Environmental effects on gene expression
c) Genetic species difference
d) Heritable DNA
Kendler et al. studied which disorder?
a) Anxiety
b) Schizophrenia
c) Depression
d) Bipolar
Neurotransmitters primarily cause:
a) Hormonal changes
b) Electrical activity
c) Chemical signalling
d) Brain restructuring
Brain development process strengthening synapses:
a) Neurogenesis
b) Long-term potentiation
c) Dendritic pruning
d) Lateralization
Evidence against strict localization shows:
a) Compartmentalized function
b) Compensation across regions
c) No neuroplasticity
d) Motor corpus callosum
Pheromones are:
a) Emotional hormones
b) Chemicals influencing mating
c) Genetic markers
d) Neurotransmitters

Which structure connects the two hemispheres of the brain?
a) Hippocampus
b) Corpus callosum
c) Amygdala
d) Thalamus
What is the primary function of the frontal lobe?
a) Auditory processing
b) Emotional regulation
c) Executive functions and decision-making
d) Visual interpretation
Which neurotransmitter is most associated with pleasure and reward?
a) Dopamine
b) Serotonin
c) GABA
d) Acetylcholine
What type of study design is typically used to compare monozygotic and dizygotic twins?
a) Correlational study
b) Twin study
c) Case study
d) Experimental design
What is the primary purpose of the limbic system?
a) Cognitive reasoning
b) Emotional processing and memory
c) Voluntary movement
d) Visual coordination
Which research method measures brain waves and electrical activity?
a) MRI
b) EEG
c) PET
d) fMRI
Which biological principle suggests that behavior has a physiological basis?
a) Evolutionary adaptation
b) Localization of function
c) Reductionism
d) Biological correlates of behavior
What does the term “neurotransmission” refer to?
a) Hormone release into the bloodstream
b) The process of neurons communicating via synapses
c) Brain imaging using magnetic fields
d) DNA replication in neurons
Which study demonstrated the relationship between cortisol levels and memory performance?
a) Antonova et al.
b) Newcomer et al.
c) Maguire et al.
d) Draganski et al.
The amygdala is most closely associated with which emotion?
a) Happiness
b) Anger
c) Fear
d) Surprise
Which of the following best defines neurogenesis?
a) Formation of new neurons
b) Removal of synapses
c) Strengthening of neural connections
d) Destruction of old brain cells
The process of strengthening neural pathways due to repeated stimulation is known as:
a) Neurogenesis
b) Neural pruning
c) Long-term potentiation
d) Localization
Which of the following is not an example of brain imaging technology?
a) MRI
b) PET
c) EEG
d) CAT
Which study provided evidence for brain changes after learning a new skill like juggling?
a) Draganski et al.
b) Maguire et al.
c) Gazzaniga and Sperry
d) Wedekind et al.
What is the main role of the hypothalamus?
a) Regulates sleep and appetite
b) Controls hormonal balance and homeostasis
c) Processes auditory stimuli
d) Integrates motor coordination
What does the “fight-or-flight” response primarily involve?
a) Oxytocin release
b) Activation of the parasympathetic system
c) Adrenaline and cortisol release
d) Neural inhibition
Which research technique is most useful for studying brain function over time without invasive procedures?
a) EEG
b) MRI
c) PET
d) fMRI
Which of the following best explains the term “genetic heritability”?
a) The extent to which traits can be learned
b) The proportion of variation in behavior explained by genes
c) The number of chromosomes in a genotype
d) The stability of gene expression across environments
In evolutionary psychology, what is a key explanation for mate selection?
a) Random mating
b) Social learning
c) Genetic diversity for survival advantage
d) Environmental conditioning
What does the principle of “reductionism” imply in biological psychology?
a) Complex behaviors can be explained by simple biological processes
b) Behavior is independent of biology
c) Brain functions are indivisible
d) Learning cannot be studied biologically

MCQ MARKSCHEME

1-b
2-c
3-c
4-c
5-b
6-b
7-c
8-c
9-b
10-b
11-c
12-c
13-b
14-c
15-b
16-b
17-b
18-c
19-b
20-a
21-b
22-d
23-d
24-c
25-b
26-c
27-c
28-b
29-b
30-b
31-b
32-c
33-a
34-b
35-b
36-b
37-d
38-b
39-b
40-c
41-a
42-c
43-d
44-a
45-b
46-c
47-d
48-b
49-c
50-a

Short Answer Questions

1. Explain one technique used to study the brain in relation to behaviour. [9]

Markscheme:

7–9: Clearly identifies a brain imaging technique (e.g., MRI, fMRI, PET, or EEG). Explains its function and how it links structure/activity to behaviour. Supports explanation with a study (e.g., Maguire et al., 2000) describing aim, method, and findings. Explicitly links how the technique demonstrates the relationship between brain and behaviour (e.g., hippocampal volume → spatial memory).
4–6: Identifies a brain scanning technique and partially explains its use. Describes a relevant study but may lack full methodological or result detail. Link between technique and behaviour is implied but underdeveloped.
1–3: Mentions a brain imaging technique or study superficially, with limited or no explanation of how it relates to behaviour.
0: No relevant response.

2. Explain one study related to localization of function in the brain. [9]

Markscheme:

7–9: Defines localization (specific brain areas perform specific functions). Describes a relevant study (e.g., Broca, Gazzaniga & Sperry, or Maguire). Accurately outlines aim, procedure, results, and conclusion. Clearly connects study findings to localization (e.g., left hemisphere = language production).
4–6: Provides basic definition and study description but connection to localization or behaviour is partially developed.
1–3: Mentions localization or a study vaguely with minimal explanation.
0: Irrelevant or no response.

3. Explain one study on neuroplasticity. [9]

Markscheme:

7–9: Defines neuroplasticity as the brain’s ability to change structure and function. Describes a relevant study (e.g., Maguire et al., 2000 or Draganski et al., 2004). Explains how experience or learning caused measurable structural change (e.g., increased hippocampal volume). Clear link between evidence and concept.
4–6: Describes the concept and study but misses key findings or full linkage.
1–3: Minimal mention of neuroplasticity or study.
0: No relevant material.

4. Explain one example of neuroplasticity in humans. [9]

Markscheme:

7–9: Defines neuroplasticity and provides a clear human example (e.g., London taxi drivers in Maguire, juggling in Draganski). Accurately describes method, findings, and how behaviour affected brain structure.
4–6: Examples provided but limited detail or partial linkage.
1–3: Superficial example with limited accuracy.
0: Irrelevant.

5. Explain one study investigating the effect of neurotransmission on behaviour. [9]

Markscheme:

7–9: Defines neurotransmission. Identifies neurotransmitters (e.g., acetylcholine, serotonin, dopamine). Describes one study (e.g., Antonova et al., 2011; Crockett et al., 2010; Fisher et al., 2005). Accurately outlines aim, method, and results. Explains how neurotransmitters influenced specific behaviour (e.g., memory, prosociality, reward).
4–6: Some correct details but incomplete explanation or weaker link to behaviour.
1–3: Mention a neurotransmitter or study superficially.
0: No relevant response.

6. Describe the role of one neurotransmitter in human behaviour. [9]

Markscheme:

7–9: Identifies neurotransmitters (e.g., acetylcholine, serotonin, dopamine). Explains its function and behavioural influence using one study. (e.g., acetylcholine → spatial memory; Antonova et al., serotonin → prosociality; Crockett et al.). Clear, accurate linkage.
4–6: Describes neurotransmitters correctly but partially links to study or behaviour.
1–3: Vague mention of neurotransmitter or incomplete study description.
0: No credit.

7. Explain one effect of a hormone on human behaviour. [9]

Markscheme:

7–9: Defines hormones and identifies one (e.g., cortisol, oxytocin, testosterone). Describes one study in detail (e.g., Newcomer et al. for cortisol; Ronay & von Hippel for testosterone; Scheele et al. for oxytocin). Links hormone’s physiological role to behavioural outcome.
4–6: Some correct details, but connection between hormones and behaviour underdeveloped.
1–3: Minimal or inaccurate explanation.
0: Irrelevant.

8. Describe one study on hormones and behaviour. [9]

Markscheme:

7–9: Study accurately described with aim, method, results, and conclusion. Hormonal mechanism (e.g., cortisol → stress and memory; oxytocin → bonding) clearly linked to behavioural change.
4–6: Study described but connection to behaviour partially developed.
1–3: Limited accuracy or superficial description.
0: No relevant response.

9. Explain one function of pheromones in human behaviour. [9]

Markscheme:

7–9: Defines pheromones as chemical signals influencing behaviour. Uses one study (Wedekind et al., 1995) to explain mate selection and MHC diversity. Fully links findings to evolutionary behaviour.
4–6: Study described but explanation of pheromone mechanism weaker.
1–3: Vague or inaccurate mention.
0: No relevant response.

10. Explain one study on the role of pheromones in human behaviour. [9]

Markscheme:

7–9: Clearly describes Wedekind et al. (1995): aim, method, findings. Explains MHC–pheromone link and its evolutionary significance.
4–6: Study described without full linkage.
1–3: Partial description or unclear concept.
0: No credit.

11. Explain one study on the effect of genes on behaviour. [9]

Markscheme:

7–9: Defines genetic influence and heritability. Accurately describes one study (e.g., Kendler et al., 2006; Caspi et al., 2003; Weaver et al., 2004). Explains how genetic or epigenetic mechanisms influence behaviour.
4–6: Study partially described; weaker connection to behaviour.
1–3: Mentions genetics superficially.
0: No relevant response.

12. Explain one evolutionary explanation of behaviour. [9]

Markscheme:

7–9: Defines evolution and natural selection. Uses one study (e.g., Wedekind et al., 1995; Buss, 1989). Clearly links behaviour (e.g., mate selection) to evolutionary advantage.
4–6: Partial understanding or study described without clear linkage.
1–3: Minimal explanation or vague reference.
0: No relevant answer.

13. Describe one ethical consideration in research into the biological approach. [9]

Markscheme:

7–9: Identifies one ethical issue (e.g., informed consent, harm, genetic data, animal welfare). Uses one study (e.g., Wedekind, Antonova, Weaver, or Ferguson) to show how the concern was/should be addressed (e.g., debriefing, risk minimisation, ethical approval).
4–6: Identifies and partly discusses issues, mentions study but limited analysis.
1–3: Superficial mention of ethics.
0: No credit.

14. Explain one study using an animal model in biological research. [9]

Markscheme:

7–9: Accurately explains use of an animal model (e.g., Weaver et al. on maternal care, Ferguson et al. on oxytocin). Describes aim, procedure, and findings. Explains relevance to human behaviour. Mentions ethical considerations (3Rs).
4–6: Study described but link to human behaviour or ethics partial.
1–3: Vague or incomplete description.
0: No relevant material.

15. Explain one ethical consideration in animal research. [9]

Markscheme:

7–9: Clearly identifies an ethical issue (e.g., harm, housing, euthanasia). Uses one animal study (e.g., Weaver or Ferguson) to discuss how ethics were/should be maintained (3Rs).
4–6: Ethical issue identified and partly discussed.
1–3: Superficial.
0: No credit.

16. Explain one study investigating neurochemical or hormonal influence on behaviour. [9]

Markscheme:

7–9: Identifies neurotransmitter/hormone; describes one relevant study (Antonova or Newcomer); accurately explains how brain chemistry affects behaviour.
4–6: Study or explanation incomplete.
1–3: Limited detail.
0: No relevant response.Excellent — we’ll continue seamlessly from Question 16, keeping the same IB-exam standard:

17. Explain one study showing how oxytocin influences human behaviour. [9]

Markscheme:

7–9: Defines oxytocin and its social role; accurately describes Scheele et al. (2012) or similar. Links increased oxytocin to monogamous or trust-related behaviour. Explicitly connects hormone mechanism with social bonding.
4–6: Correct hormone identified, study described briefly or link under-developed.
1–3: Mentions oxytocin or bonding vaguely, little supporting detail.
0: Irrelevant.

18. Explain one study on testosterone and behaviour. [9]

Markscheme:

7–9: Defines testosterone and its association with dominance or risk-taking. Fully describes Ronay & von Hippel (2010) – skateboard task, male risk behaviour, social context. Explains causal relation between testosterone levels and competition display.
4–6: Partial explanation or incomplete description of findings.
1–3: Mentions testosterone or risk-taking without detail.
0: No credit.

19. Explain one study on the role of serotonin in behaviour. [9]

Markscheme:

7–9: Identifies serotonin as a mood-regulating neurotransmitter. Describes Crockett et al. (2010) or similar; shows link between increased serotonin and prosocial moral decision-making.
4–6: Study described but partial linkage or missing mechanism.
1–3: Mentions serotonin or study superficially.
0: Irrelevant.

20. Explain one study on dopamine and reward-related behaviour. [9]

Markscheme:

7–9: Defines dopamine and its role in motivation/reward. Uses Fisher, Aron & Brown (2005) – fMRI evidence of dopamine activity in romantic love. Clear link between mesolimbic dopamine pathway and reward feelings.
4–6: Correct study, partial description or weak connection.
1–3: Minimal mention of dopamine or incomplete study.
0: No relevant response.

21. Explain one study on the relationship between brain and behaviour using fMRI. [9]

Markscheme:

7–9: Describes fMRI as functional imaging showing blood-oxygen levels; applies Antonova et al. (2011) or Fisher et al. (2005). Accurately links observed brain activation to specific behaviour (memory or emotion).
4–6: Technique identified, study partly described.
1–3: Mentions fMRI vaguely.
0: Irrelevant.

22. Explain one study showing interaction between environment and brain structure. [9]

Markscheme:

7–9: Defines interactionist view; uses Rosenzweig & Bennett (1972) or Draganski et al. (2004). Describes enriched vs deprived environments and resulting cortical or grey-matter change.
4–6: Partial description or weaker link between environment and neural change.
1–3: Superficial mention of environment or study.
0: No credit.

23. Explain one study showing gene–environment interaction on behaviour. [9]

Markscheme:

7–9: Describes interaction concept; uses Caspi et al. (2003) – 5-HTT gene × life stress predicting depression. Details procedure and shows moderation effect.
4–6: Some accurate detail but partial linkage.
1–3: Mentions gene or environment superficially.
0: No relevant material.

24. Explain one twin study investigating genetic influences on behaviour. [9]

Markscheme:

7–9: Defines MZ/DZ twins; describes Kendler et al. (2006) – heritability of depression. Presents concordance results and explains genetic contribution.
4–6: Study partly described, weaker linkage.
1–3: Minimal reference.
0: Irrelevant.

25. Explain one cross-cultural study supporting evolutionary explanations of behaviour. [9]

Markscheme:

7–9: Uses Buss (1989) – 37 cultures, mate preferences (resources vs youth). Links patterns to reproductive fitness.
4–6: Study described but evolutionary link partial.
1–3: Minimal mention.
0: Irrelevant.

26. Explain one limitation of using animal models to study human behaviour. [9]

Markscheme:

7–9: Identifies generalisation issue; uses Ferguson et al. (2000)* or Weaver et al. (2004)* to illustrate similarities/differences in physiology or ethics. Evaluates translational value.
4–6: Limitation identified, discussion partial.
1–3: Superficial comment.
0: None.

27. Explain one ethical consideration when using animals in biological research. [9]

Markscheme:

7–9: Identifies issue (harm, housing, euthanasia). Applies Weaver et al. or Rosenzweig & Bennett to show how 3Rs were/should be followed.
4–6: Issue identified, partly explained.
1–3: Superficial.
0: No relevant content.

28. Explain one ethical consideration in human biological research. [9]

Markscheme:

7–9: Identifies issue (informed consent, deception, distress, genetic data). Illustrates with Antonova et al. (drug administration) or Wedekind et al. (scent exposure). Explains mitigation (debriefing, anonymity, consent).
4–6: Issue stated, discussion limited.
1–3: Superficial reference.
0: Irrelevant.

29. Explain one study showing neuroplasticity after brain injury or training. [9]

Markscheme:

7–9: Defines neuroplasticity; uses human example (Maguire, Draganski) to show adaptation post-experience. Connects structural change to functional recovery.
4–6: Partial development.
1–3: Minimal.
0: None.

30. Explain one way technology has advanced understanding of brain and behaviour. [9]

Markscheme:

7–9: Identifies technology (MRI/fMRI/PET/EEG); explains advantages (non-invasive, spatial resolution). Illustrates with Maguire et al. or Antonova et al.; links technological insight to understanding localisation or neuroplasticity.
4–6: Technique identified, benefits partly explained.
1–3: Vague.
0: No credit.

31. Explain one limitation of localisation of function research. [9]

Markscheme:

7–9: Discusses assumption of strict localisation vs distributed processing. Uses Maguire or Gazzaniga & Sperry to illustrate plasticity/compensation.
4–6: Limitation identified but under-developed.
1–3: Brief.
0: No relevant content.

32. Explain one ethical consideration in genetic research. [9]

Markscheme:

7–9: Identifies issue (privacy, informed consent, predictive harm). Illustrates with Kendler et al. or Caspi et al. Discusses how confidentiality and counselling are ensured.
4–6: Issue identified, partly discussed.
1–3: Superficial.
0: No relevant response.

Essay Response Questions

1. To what extent does brain localisation influence behaviour? [22]

Markbands:

1–7: Minimal or inaccurate understanding of localisation; vague description of brain regions; minimal or no use of research. No reference to studies such as Broca, Wernicke, Gazzaniga, or Maguire. No critical discussion of distributed processing or neuroplasticity.
8–14: Adequate description of localisation and at least one relevant study (e.g. Broca or Gazzaniga). Some accurate explanation but lacking depth or critical evaluation. Limited structure.
15–19: Good understanding of localisation; accurate reference to two or more studies (e.g. Maguire’s hippocampus study + Gazzaniga’s split-brain work). Some evaluation of strengths and limitations of localisation (e.g. compensatory functions, individual variability). Clear organisation.
20–22: Comprehensive analysis of localisation and its limits. Multiple studies integrated and critically compared. Discusses plasticity, network theories, or distributed processing as alternative views. Sophisticated, balanced conclusion; well-organised structure.

2. Discuss the role of brain imaging technologies in investigating the relationship between biology and behaviour. [22]

1–7: Descriptive list of technologies (e.g. MRI, fMRI, PET) with no clear link to behaviour or research evidence.
8–14: Describes two techniques with some accurate information. Limited linkage to studies (e.g. Maguire, Antonova) and minimal analysis.
15–19: Good explanation of multiple imaging techniques (MRI, fMRI). Research (Maguire, Fisher, Draganski) accurately described and clearly connected to behaviour. Partial evaluation of advantages and limitations (resolution, ecological validity).
20–22: Comprehensive understanding of multiple techniques. Integrates studies to evaluate their contributions and limitations. Critical discussion of reliability, validity, ethics, and triangulation. Clear structure with conclusion.

3. Evaluate the role of neuroplasticity in human behaviour. [22]

1–7: Vague understanding of neuroplasticity; may confuse with localisation. Minimal research support.
8–14: Adequate definition; describes one relevant study (Maguire or Draganski). Some link between experience and brain change. Limited analysis of implications.
15–19: Good understanding supported by at least two studies (Maguire, Draganski, Rosenzweig). Evaluation of strengths and weaknesses (correlational, causal ambiguity). Discusses real-world relevance (rehabilitation, learning).
20–22: Thorough analysis of neuroplasticity and its implications for human behaviour. Integrates multiple studies with critical evaluation. Discusses bidirectional brain–behaviour relationship, individual differences, and methodological rigor. Excellent structure.

4. Evaluate the role of neurotransmission in human behaviour. [22]

1–7: Minimal knowledge of neurotransmitters. No or vague study reference.
8–14: Describes one neurotransmitter (e.g. acetylcholine or serotonin) with one supporting study (Antonova, Crockett). Partial understanding of mechanism.
15–19: Good explanation using two neurotransmitters (acetylcholine, serotonin, dopamine). Studies described accurately with behavioural linkage. Evaluation considers reductionism and methodological limitations.
20–22: Comprehensive evaluation of multiple neurotransmitters and behaviour. Integrates contrasting studies. Discusses complexity of neurotransmission (interaction, receptor sensitivity, individual variation). Balanced, well-organised argument.

5. Discuss the role of hormones in human behaviour. [22]

1–7: Basic or inaccurate understanding of hormones; no research or unclear linkage to behaviour.
8–14: Describes one hormone (e.g. cortisol, oxytocin, or testosterone) and one study (Newcomer, Ronay & von Hippel, or Scheele). Some relevance to behaviour.
15–19: Good explanation of multiple hormones; studies well described and linked to behavioural outcomes. Some evaluation of causality and ethical constraints.
20–22: Comprehensive, comparative discussion of hormonal influence on behaviour. Integrates multiple studies and critically evaluates findings (temporal effects, individual variation, measurement challenges). Clear structure and conclusion.

6. Evaluate research on pheromones and their possible effects on human behaviour. [22]

1–7: Minimal understanding of pheromones; inaccurate examples.
8–14: Describes Wedekind et al. (1995) or similar research; basic link between pheromones and mate selection.
15–19: Good explanation with critical discussion of methodology (artificial setting, sample bias). May reference follow-up studies.
20–22: Excellent evaluation of pheromone research. Integrates findings, limitations (replicability, alternative explanations, human olfactory complexity). Discusses evolutionary basis and ethical considerations. Logical structure.

7. To what extent do genetic factors influence behaviour? [22]

1–7: Limited or inaccurate understanding of genetics. Minimal or irrelevant research.
8–14: Basic discussion with one study (Kendler, Caspi). Some awareness of heritability or gene–environment interaction.
15–19: Good explanation using two or more studies (Kendler, Caspi, Weaver). Integrates gene–environment and epigenetic findings.
20–22: Sophisticated, critical discussion of genetic influence. Evaluates twin, adoption, and molecular research. Integrates epigenetic findings and ethical considerations. Well-organised and balanced argument.

8. Discuss the role of evolution in behaviour. [22]

1–7: Limited description of evolution, inaccurate examples.
8–14: Describes one study (Wedekind or Buss) with basic evolutionary explanation.
15–19: Good explanation using two studies (Wedekind, Buss). Discusses natural/sexual selection. Some evaluation of cultural and methodological limitations.
20–22: Comprehensive discussion of evolutionary explanations. Critically evaluates evidence (cross-cultural issues, ethics, post-hoc reasoning). Clear synthesis and structure.

9. Evaluate research into the use of animal models in biological research. [22]

1–7: Minimal description or inaccurate information about animal research.
8–14: Describes one study (Weaver or Ferguson) and identifies ethical or generalisation issues.
15–19: Good understanding supported by multiple studies. Evaluates validity, ethics (3Rs), and translational limits.
20–22: Comprehensive analysis integrating methodological and ethical evaluation. Balanced discussion of advantages (control, causality) vs limitations (species differences). Coherent argument.

10. Discuss the interaction between genetic and environmental factors in behaviour. [22]

1–7: Minimal understanding; may mention “nature–nurture” without detail.
8–14: Some accurate explanation of gene–environment interaction; references Caspi et al. or Weaver.
15–19: Good explanation using multiple studies showing interplay. Evaluates methodology and implications.
20–22: Comprehensive evaluation of gene–environment interplay. Integrates twin, epigenetic, and molecular evidence. Discusses diathesis–stress model and ethics. Clear, logical structure.

11. Evaluate the use of brain imaging technology in biological research. [22]

1–7: Descriptive; no evaluation.
8–14: Accurate description of one or two technologies; limited evaluation.
15–19: Good use of research to support (Maguire, Fisher). Some discussion of strengths and weaknesses.
20–22: Critical and comparative evaluation of techniques. Considers triangulation, validity, cost, and ethics. Excellent synthesis.

12. Discuss ethical considerations relevant to the study of the brain and behaviour. [22]

1–7: Minimal reference to ethics or relevant research.
8–14: Identifies ethical issues (informed consent, risk, anonymity). Describes one study (Antonova or Maguire).
15–19: Good discussion with multiple studies. Evaluates ethical safeguards and trade-offs in biological research.
20–22: Comprehensive evaluation of ethical concerns (neuroimaging, drug use, incidental findings). Integrates ethics into argument. Coherent and balanced.

13. To what extent does the biological approach explain human behaviour? [22]

1–7: Descriptive, inaccurate, or one-dimensional.
8–14: Outlines basic principles and provides one or two examples.
15–19: Well-developed discussion using studies from localisation, hormones, or genetics. Notes reductionism vs interactionism.
20–22: Sophisticated evaluation of biological approach. Integrates biological and cognitive/sociocultural perspectives. Discusses ethics and methodological implications. Strong conclusion.

14. Discuss the role of hormones and neurotransmitters in behaviour. [22]

1–7: Minimal or confused understanding.
8–14: Basic description of one neurotransmitter and one hormone with partial explanation.
15–19: Good understanding using multiple studies (Antonova, Crockett, Newcomer, Ronay).
20–22: Comprehensive integration of both systems. Evaluates interplay, causality, and methodological constraints. Well-structured essay.

15. Discuss how the biological approach is demonstrated in research. [22]

1–7: Minimal understanding of the biological approach.
8–14: Some accurate examples from biological studies.
15–19: Good range of examples across subtopics (localisation, neurotransmission, hormones).
20–22: Comprehensive synthesis showing principles through multiple studies. Evaluates strengths and limitations. Clear structure.

16. Evaluate the role of animal research in understanding hormones and behaviour. [22]

1–7: Limited description or irrelevant example.
8–14: Describes one animal study with partial relevance.
15–19: Accurate description of several studies (Ferguson, Weaver). Evaluates generalisability and ethics.
20–22: Thorough analysis of how animal research informs human understanding. Balanced ethical and methodological discussion. Clear and critical argument.

17. Evaluate one or more studies investigating neuroplasticity. [22]

1–7: Minimal or inaccurate reference to studies.
8–14: Describes one study (Maguire or Draganski).
15–19: Accurate description and evaluation of multiple studies.
20–22: Integrates research and evaluates design, causality, ethics, and real-world application. Clear and logical essay.

18. Evaluate the strengths and limitations of the biological approach to understanding behaviour. [22]

1–7: Minimal understanding; may list unrelated studies.
8–14: Some understanding of key ideas and relevant examples.
15–19: Well-developed explanation using multiple studies. Evaluates reductionism, determinism, and ethics.
20–22: Comprehensive and balanced evaluation. Integrates multiple subtopics, discusses triangulation and complementarity with other approaches. Excellent organisation.