BEHAVIORAL GENETICS PSYCH 3102 Dr Hewitt
HOMEWORK # 5 and PRACTICE EXAM III.
moderate retardation Down syndrome mild retardation dementia
severe retardation reading disorder fragile X syndrome PKU
dyslexia Alzheimers disease Lesch-Nyhan syndrome
additive gene effects non-additive gene effects genotype x environment interaction
assortative mating random mating inbreeding depression
Subaverage intellectual functioning, IQ in the range 35-50 moderate retardation
Subaverage intellectual functioning, 85% of the retarded mild retardation
Metabolic disorder causing moderate retardation if untreated PKU
Second most common genetic cause of retardation fragile X
Category comprising 80% of learning disorders reading disorder
Severe cognitive decline with age dementia
Specific type of reading disorder dyslexia
Lowering of mean phenotypic score often seen in the offspring
of related individuals inbreeding depression
Disease causing 50% of dementia cases Alzheimers disease
A cause of correlation between spouses assortative mating
Effect seen when changes caused by the environment depend
on the genotype of the individual genotype/environment interaction
Give reasons for your answer. Prevalence of autism is only 0.045% (4 or 5 per 10,000) but risk is 3%. Risk is therefore 60 times prevalence, indicating strong family resemblance – family members are 60 times more likely to have autism than members of the general population.
Condition MZ correlation DZ correlation
ADHD 0.62 0.25
Depression 0.44 0.19
Autism 0.91 0.44
moderate heritability of 62% ( from MZ twin correlation)
non-shared e accounts for 38% of variation (from MZ correlation)
no evidence for shared e since DZ correlation is not more than half the MZ correlation
some evidence for non-additive gene effects since DZ correlation is less than half MZ correlation
lower heritability than ADHD, h2= 44% (from MZ correlation)
biggest influence on variation = non-shared e at 56% (from MZ correlation)
no evidence of shared e (MZ correlation> DZ correlation x2)
DZ correlation indicates may be some non-additive gene effects.
highest heritability of the 3 disorders here, heritability = 91%
very little non-shared e (9% of variance)
no evidence for shared e or non-additive gene effects since MZ correlation = 2 x DZ correlation
____any from class eg Down syndrome, Turners_syndrome___________
ii Name a single gene disorder that is a cause of mental retardation
_____any from class eg PKU, Duchenne muscular dystrophy etc__________
iii Is there any evidence that the genes involved in these disorders have an effect on cognitive ability in the normal range? Give reasons for your answer.
depends on which disorders you chose as examples
eg Down syndrome – yes, there does appear to be at least one gene for cognition on chromosome21, in the DownCriticalRegion1, recognized so far
PKU – no, the PKU locus does not appear to be a gene that normally functions in cognitive processes in the brain.
What is g? general measure of cognitive ability derived by factor analysis from scores from tests of various more specific abilities whose scores intercorrelate
Explain the evidence for a genetic influence on g from the following:
parent/offspring correlations are in the range of 0.42 – 0.47
indicates level of cognitive ability does run in families
but this could be due to shared e or shared genes or both
adopted apart P/O and sib correlations = 0.24, indicating heritability of 48%
adoptive P/O and sibs correlate in range 0.19 – 0.32, indicating shared e component of 19 – 32% of the variation.
MZ correlation = 0.86 DZ = 0.60
indicates heritability of 52%, shared e (34%) and non-shared e (14%) as influences also
Summarize the factors influencing g in childhood
all data is consistent with heritability of about 50%, shared e = 25% and non-shared e (and error) = 25% of variance during childhood
How do these influences change over time?
shared e influence does not persist and heritability gets bigger:
60+% of variation in adulthood is genetic, rest of variation is non-shred e (and error)