Biological Explanations of Schizophrenia

Question 1

What are the key points of the genetic explanation ?

Answer 1

• Family studies
• Twin studies
• adoption studies
• candidate genes
• polygenic
• aetiologically Heterogenous

Question 2

What are the 2 biological explanations of schizophrenia ?

Answer 2

1. Genetic
2. Neural correlate (dopamine)

Question 3

What are family studies and twin studies used for and give an example of a first and second degree relative ?

Answer 3

They are used to look at the genetic basis of schizophrenia by comparing concordance rates
First - Parent, sibling
secondary- Grandparents aunties

Question 4

What are adoption studies used for?

Answer 4

As adopted children grow up in a different environment to their biological parent, we can compare genetics and see if environment plays a part.

Question 5

What Is a candidate gene?

Answer 5

A gene that is involved with the development of schizophrenia - gives the individual a genetic vulnerability to developing it

Question 6

What is meant by polygenic ?

Answer 6

A condition with many potential genes

Question 7

What is meant by schizophrenia being aetiologically heterogenous ?

Answer 7

Different combinations of factors, including genetic variation, lead to the condition

Question 8

What is the role of mutation in the development of schizophrenia ?

Answer 8

Schizophrenia can have a genetic origin in the absence of a family member with the disorder. This could be from a mutation in parental DNA which can be caused by poison, viral infection and radiation.

Question 9

AO3 - study of relations

Supporting evidence for the genetic explanation

Answer 9

Riley and Kendler - the lifetime risk for developing it is around 1% but its 10x greater when you have a first degree relative with the disorder

Gottesman - large scale family study showed that if someone had an :
aunt- they had a 2% chance of developing it
Sibling - 9% chance
identical twin - 48% chance

Question 10

AO3 - Candidate genes

Answer 10

Ripke et al - combined all previous data from genome-wide studies. He compared the genetic make-up of 37,000 people with schizophrenia with 113,000 controls
- He found 108 genetic variations were associated with slightly increased risk e.g PCM1 gene

Question 11

What are the key points of the neural explanation ?

Answer 11

Neurotransmitters as a cause for schizophrenia - dopamine

Structure and functional differences of the brain

Question 12

What is the neurotransmitter involved in the development of schizophrenia ?

Answer 12

Dopamine

Question 13

Describe the neurotransmitter dopamine and research about it

Answer 13

It’s a monoamine neurotransmitter which is converted to DOPA and decarboxylated into dopamine.

Once it’s released into the synaptic cleft it’s absorbed by receptors. There are 5D receptors each with a different function and found in different locations

Owen et al - found increased D2 receptors in people with schizophrenia

Lindstroem et al - Chemicals needed to produce dopamine are taken up much faster in people with schizophrenia

Question 14

What is meant by hyperdopaminergia?

Answer 14

Too much dopamine

Question 15

What is meant by hypodopaminergia?

Answer 15

Too little dopamine

Question 16

Outline the original dopamine hypothesis

Answer 16

High levels of dopamine in the subcortical areas of the brain (inner part of the brain- mesolimbic pathway)

Only takes into account positive symptoms

Hyperdopaminergia
This increases the positive symptoms

Question 17

What did Falkai et al find about the original dopamine hypothesis ?

Answer 17

Found increased dopamine in the left amygdala of schizophrenic patients post mortem

Question 18

What do amphetamines do?

Answer 18

Increase dopamine levels

Question 19

What does the drug L-Dopa do?

Answer 19

Increase dopamine levels

Question 20

What do anti-psychotics do?

Answer 20

Decrease dopamine levels

Question 21

What does Curren et al say in terms of dopamine?

Answer 21

Amphetamines increase dopamine levels which worsens schizophrenic symptoms and inducing them in those without it

Question 22

What does Tenn et al say in terms of dopamine?

Answer 22

Used amphetamines to induce schizophrenic like symptoms in rats and then reduced them by using drugs that reduces dopamine

• supporting that increased dopamine causes schizophrenia

HOWEVER

anthropomorphism - you can’t generalise these findings onto humans as we are different

Question 23

Outline the updated dopamine hypothesis

Answer 23

Davis et al -

High and low levels of dopamine in different areas of the brain are responsible for different symptoms

Mesocortical pathway - outside part of the brain, too little dopamine (hypodopaminergia), leads to negative symptoms, aim of treatment is to increase dopamine levels

Mesolimbic pathway - Inner part of the brain, too high levels of dopamine (hyperdopaminergia), leads to positive symptoms, aim of treatments is to reduce dopamine levels

Question 24

Research that limits both of the dopamine hypothesis’

Answer 24

McCutcheon et al -

live-scanning and post mortem have consistently shown differing levels of glutamate (neurotransmitter that affects memory, learning and attention) in those with schizophrenia - dopamine isn’t the only neurotransmitter implicated

Depatie and Lal -

The drug apomorphine increases dopamine levels but has not been found to induce schizophrenic like symptoms

Question 25

What are some brain (neurological) abnormalities in people with schizophrenia ?

Answer 25

- Enlarged Ventricles - Ventricles containing cerebrospinal fluid which 'flushes out' the brain during REM sleep become enlarged - Reduced grey matter - Enlarged ventricles leads to reduced grey matter and functioning neurons in the temporal and frontal lobes and the thalamus - Smaller brain size - Less grey matter so have a smaller brain but the shrinkage stops when anti-psychotics are introduced in the brains of people with schizophrenia, ventricles become Enlarged. This leads to a reduction in grey matter making their brains 2.6% smaller according to Haijma et al. (2013) and 6% lighter according to Brown et al (1986). Therefore functional neurons, in the temporal lobes (verbal and acoustic memory), the frontal lobes (planning and coordination) and thalamus (integrating sensory and motor information) are affected . Haijma et al. (2013) found a smaller thalamus in their MRI study. However, this shrinkage stops when anti-psychotics are introduced.

Question 26

What did Juckel et al find?

Answer 26

Avolition is negatively correlated with the ventral striatum (a primitive reward centre in the brain) as he found lower activity in schizophrenics than the control group

Question 27

What did Allen et al find?

Answer 27

Scanned patients with auditory hallucinations, compared to a control. lower activation levels were found in the superior temporal gyrus (auditory processing) and anterior cingulate gyrus (involved in emotion regulation, decision-making and error detection) of hallucination group.