Lesson 2

Question 1

genetic basis

Answer 1

Family studies- find individuals who have sz and whether their biological relatives are similarly affected more often then non-biological, have shown the closer genetic relatedness the greater the risk, Gottesman 1991found it both parents were sz then the likelihood of offspring having it was 46%, if one parent sz likelihood dropped to 13%, if sibling had sz likelihood was 9%
Twin studies- investigate nature/nurture debate in terms of contribution of heredity and environmental influences, if sz is genetic then concordance rates should be higher for mz twins than dz, Gottesman 1991 found 48% concordance rate for mz twins and 17% for dz twins, Joseph 2004 reviewed twin studies carried out up to 2001, found overall concordance rate for mz twins as 40% but 4.7% for dz twins
Adoption studies- difficult to separate genes and environment in other studies so carried out to understand nature/nurture influence, mz twins reared apart/offspring of sz parents adopted, Tienari et al 2001study in Finland, 164 adoptees whose biological mothers diagnosed with sz, 11 (6.7%)were also diagnoed with sz compared to control group of 197 where only 4 (2%)were diagnosed, still small link between genes

Question 2

candidate genes

Answer 2

-specific genes associated with sz, now agreed sz is polygenic- combination of different genes implicated in sz
-Ripke et al 2014 compared genetic makeup of 37000 sz patients worldwide with 113000 controls, found 108 separate genetic variations were associated with increased risk of sz
genes particularly vulnerable were ones that had some connection to functioning of certain neurotransmitters such as dopamine

Question 3

genetic basis evaluation

Answer 3

-lots of research support for genetic basis, Gottesman joseph and tiernari, shows that if a child grows up in family where both parents have sz chances of them getting it is heightened
-problem with family and twin studies is separating nature and nurture, eg mz twins normally reared the same way dofficult to separate genes and upbringing, in adoption studies children tend to be adopted by relatives who may raise the child similarly, may not be a good comparison
-sz can take place in absence of family history, may be a mutation in eg paternal sperm cells caused by radiation, poison, infection, Brown et al 2002 showed positive correlation between paternal age and increased risk of sz, 0.7% in fathers under 25 to over 2% in fathers over 50, suggests though no direct genes involved person can still get sz if father was older at fertilisation, nature and nurture rather than just genes
-diathesis stress model states there is a genetic vulnerability in sz but is only likely to be triggered if there is a stress-trigger in the individuals life, need to be cautious when looking at genetic factors since may not trigger sz alone

Question 4

neural correlates

Answer 4

-measurements of the structures of function of the brain that have a relationship with sz, especially different regions of the brain, also refers to how different neurotransmitters in different parts of the brain can play a part in sz
Dopamine hypothesis- claims that an excess of dopamine in certain regions of the brain is associated with positive systems of sz, thus messages from neurons that transmit dopamine fire too easily and often, leading to hallucinations and delusions, sz thought to have particularly high levels of d2 receptors on receiving neurons resulting in more dopamine binding therefore more neurons firing

Question 5

consequences of dopamine hypothesis

Answer 5

Hyperdopaminergia in the subcortex- original version, states there are high levels of activity of dopamine in an area of the brain known as subcortex(central areas), eg excess of dopamine receptors in brocas area may be associated with speech problems/auditory hallucinations
Hyperdopaminergia in cortex- revent versions focus on lower levels of dopamine in cortex, Goldman-Rakic et al 2004 focused on role of low levels of dopamine in prefrontal cortex on negative symptoms of sz
-suggested that cortical hyperdopaminergia leads to subcortical

Question 6

neural correlates evaluation

Answer 6

-supported by drug research, dopamine agonists like amphetamines tend to increase dopamine levels and worsen sz symptoms and produce in non-patients
-Tauscher et al 2014, antipsychotics act like antagonists, reduce levels in sz patients, supports idea dopamine is high in sz patients and can be reduced through drugs
-Lindstroem et al 1999, found chemicals needed to produce dopamine are taken up faster in brains of sz compared to controls
-dopamine hypothesis cannot be sole explanation for sz, biological and psychological factors need to be considered
-Moghadamm and Javitt 2012, more recent research focused on glutamate, another neurotransmitter implicated in sz, suggests might not just be dopamine
-correlation-causation, cuase anf effect not clear, neither is reason for correlation between levels of dopamine and sz,