The biological and genetic explanations for Sz

define biological explanations

emphasise the role of inherited factors and dysfunction of brain activity in the development of a behaviour or mental disorder

what is the dopamine hypothesis?

claims that excess dopamine in certain regions of the brain is associated with the positive symptoms of Sz

what are genetics?

inherited factors make certain individuals more likely to develop a behaviour or mental disorder

what are neural correlates?

patterns of structure/activity in the brain that correlate with Sz

what are genes?

strands of DNA which are code for your genotype

what happens to a mutated gene?

changes their coding or switch on/off

why do genes mutate?

often in response to the environmental factors

what is polygenic?

requires a number of factors to combine in order for Sz to develop

what is aetiologically heterogeneous?

different patients all have a different combination of factors hat lead to their Sz

what are candidate genes?

a gene that is believed to be related to a particular trait, such as a disease or a physical attribute

what did Gottesman find the concordance rates in Dz twins to be?

17%

what did Gottesman find the concordance rates in Mz twins to be?

48%

what did Gottesman find the concordance rates in children who’s parents both had Sz be?

46%

what did Gottesman find the concordance rates in children who had one parents with Sz to be?

13%

what are 3 supporting evidence for genetic factors of Sz?

1. family studies

2. twin studies

3. adoption studies

what have family studies established?

that Sz is more common among biological relatives of a person with Sz and that the closer the degree of genetic relatedness, the greater the risk

who conducted a family study?

grottesman

what do twin studies suggest?

if Mz twins are more similar that Dz then this suggests that the greater similarity is due to genetic factors

who did a twin study?

joseph

what did Joseph calculate?

the pooled data for all Sz twin studies carried out prior to 2001 showed a concordance rate for Mz twins of 40.4% and 7.4% for Dz

Who carried out an adoption study?

Tienari

where did Tenari conduct his adoption study?

finland

how may adoptees were involved in Tienari’s study?

164

what were the results of Tienari’s study?

• 6.7% of adoptees whose biological mothers had been diagnosed with Sz also received a diagnosis of Sz

• whereas 2% of the control adoptees received a diagnosis of Sz

how many adoptees were in Tienari’s control group?

197 whose mother didn’t have Sz

what did Tienari conclude?

the findings showed that the genetic liability to Sz had been ‘decisively confirmed’

what is the assumption of twin studies?

the environments of Mz twins and Dz twins are the same

what does the limitation suggest about twin studies?

that differences in concordance rates between Mz and Dz twins reflect nothing more than the environmental differences rather than genetic basis

what is a limitation of adoptions studies?

placement isn’t random, parents willing to take on a child with Sz mothers may be different from those unwilling to, parenting styles may therefore play a role in the development of Sz

what are the statistics of the ages of fathers at conception and the risk of Sz?

• under 25 0.7% risk

• 50+ 2% risk

what does the positive correlation between the age of fathers at conception and the risk of Sz therefore mean?

supports the genetic basis of Sz

what’s the nature nurture debate of Sz?

Sz does run in families, but it could also be due to family culture not genes

what do D2 receptors have in relation to Sz?

Sz patients dough to have abnormally high numbers of D2 receptors on receiving neurons

what do more D2 receptors mean?

more dopamine binding and triggering firing of neuron

what have PET scans shown in relation to Sz?

chemicals which are needed to manufacture dopamine are taken up faster in brains of Sz patients

where does the evidence supporting the dopamine hypothesis come from?

the success of drug treatments and that attempt to change levels of dopamine activity in the brain

What did Leucht do?

carried out a meta-analysis of 212 studies

what did the meta analysis of Leucht conclude?

that all the antipsychotic drugs tested in these studies were significantly more effective than placebo in the treatment of positive and negative symptoms, achieved by reducing the effects of dopamine

what’s a limitation of Leucht’s study?

a complex pitcher correlation does not equal causation

what is hyperdopaminergia?

too much dopamine in Broca’s and Wernicke’s area

what are excess dopamine receptors in broca’s area associated with?

alogia and auditory hallucinations

What are amphetamines?

dopamine agonists

what can Amphetamines do?

can trigger Sz symptoms hallucinations, delusions etc in non suffers and make Sz worse in Schizophrenics

What is L-dopa?

a drug for parkinson’s disease

what does L-dopa do?

increases dopamine and can trigger Sz symptoms

What are anti-psychotics?

dopamine antagonists

what do anti-psychotics do?

block dopamine receptors

what are the side effects of anti psychotics?

Parkinson type symptoms like muscle tremors

what is hypodopaminergia?

too little dopamine in the pre-frontal cortex

What is the role of glutamate?

exists as a free amino acid and is critical to mood, cognition and learning, regulates dopamine adn serotonin release and is used to manufacture GABA

what is GABA?

an inhibitory neurotransmitter

what is the most excitatory neurotransmitter in the brain?

glutamate

what receptors do glutamate bind to?

NMDA receptors

who looked at neural correlates for positive symptoms (auditory hallucinations)

Allen

who looked at neural correlates for negative symptoms (avolition)?

Juckel

what was Allen’s procedure?

scanned the brains o patients experiencing auditory hallucinations adn compared them to a control group hipster they identified pre recorded speech as theirs or others

what were the results of Allen’s study?

lower levels of activity in the superior temporal gyrus and anterior cingulate gyrus were found in the hallucinations group that made more errors

what are the limitations for Allen’s study?

• causation problems - unusual activity in those regions cause the symptoms or the other way around

• The importance of dopamine in Sz (dopamine hypothesis)

What did Juckel suggest?

a loss of motivation is due to a loss of expectation of reward for doing something

what is the ventral striatum believed to be involved in?

anticipation

what was Juckel’s procedure?

measured activity levels in the ventral striatum in Sz

what did Juckel find?

• found lower levels of activity in the lateral pre frontal cortex and ventral striatum in pps with Sz than control groups

• the lower the activity the worse the negative symptoms

what is the evaluation for Juckel

• causation problem

• dopamine hypothesis is another explanation