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Psychology 3229A/B Study Guide - Quiz Guide: Limk1, Foxp2, Language Disorder


Department
Psychology
Course Code
PSYCH 3229A/B
Professor
Scott Mac Dougall- Shackleton
Study Guide
Quiz

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Evolution & Human Behaviour
Quiz #2 Study notes
Karmiloff-Smith
Modularity of the mind
Evidence taken from patients who have lesions in specific brain regions &
specific impairments (which leave other modalities relatively unharmed);
“double dissociation” logic
Studies first done on adults; later done in children
William’s syndrome (children)
Caused by deletion of 28 genes on one copy of chromosome 7
Proficient with language & face-processing; mean IQ of 58 & severely
impaired spatial & numerical cognition
Similar claims made with specific language impairment (SLI), and
prosopagnosia (inability to recognize familiar faces)
Suggests that there are no interactions in the brain
Neuroconstructivist approach
Must take into account ontogenetic development; claimed
“modularity” that exists in adults doesn’t seem to exist in children
Prosopagnosia: face-processing deficit was ALWAYS
accompanied by object-processing deficits; thus the
independence of these two modalities seems to develop
gradually
SLI: seems to stem from lower-level cognitive impairments and
domains once thought to be normal now present with subtle
impairments (i.e. even when IQ falls in normal range, it is
significantly lower than that of siblings
William’s syndrome: intactness of spared domains challenged
on 5 counts:
1. Although they present with standard face-processing
scores, the way they achieve their success is radically
different
2. Facial & spatial processing both impaired the same way,
but the deficit is more salient for spatial stimuli
3. Many studies now challenge the “intactness” of language
module (through abnormal brain processing mechanisms)
Late language onset
Rely more on perception than language when
identifying objects
Impaired categorization abilities
Atypical pointing/gazing in toddlers
Normal asymmetry between comprehension &
production is absent in WS
4. Atypical eye movement planning; these deficits outside the
language domain could, through development, lead to the
deficits seen in WS
Genetic underpinnings of cognitive modules
Believed that mutations/problems with genes have DIRECT effects on
behaviour
KE family
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Point mutation on FOXP2 gene (encodes a transcription factor) on one
copy of chromosome 7
Mutations to the WS critical region
Mutations to elastin (involved in building of connective tissue; maybe
responsible for supravalvular stenoses seen in WS patients) and LIMK1
(protein kinase involved in spatial processing)
Neuroconstructivist approach
People with FOXP2 mutations show other deficits, not just the one in
language
Problems with LIMK1 conclusions
Mouse model knocked out 1 gene, but WS involves knockout of
28 genes
LIMK1 expressed throughout the brain, so its function appears to
be much more general
Evolutionary underpinnings of cognitive modules
FOXP2 well conserved in primates; only 2 amino acid changes in human
lineage compared to the chimps
Change thought to have occurred about 20,000 years ago (just when
language is thought to have originated)
Therefore, change of one amino acid responsible for the development
of human language
Neuroconstructivist approach
FOXP2 is a transcription factor & affects many other genes
Research on FOXP2 expression in songbirds found that FOXP2
expression was higher when the song was being learned than when it
was being produced; suggests that FOXP2 plays a role in vocal
plasticity, not language
Evolution produces allelic changes that increase an organism’s
plasticity to learning
Direct mappings of genes to cognitive-level outcomes isn’t possible; neonatal brain
is highly connected, which discredits the idea of modularity
Pinker
Three laws of behavioural genetics; thought to apply most strongly during
childhood, when our intellects/personalities are formed
1. All human behavioural traits are heritable
Note that IQ & personality tests have been shown to be quite valid
Heritability: proportion of variance in a trait (for a specific population)
that is accounted for by genetic differences
Measured using (I) twin studies, and (II) family studies
Typically range from 0.25 to 0.75
Problems with heritability
Whether measurement error is included in total variance
Additive or interactive effects as well?
Total variance can vary
When the trait is measured during ontogeny
Which population is being studied
Underlying talents & temperaments (i.e. how religious/political you are)
that lead to certain behaviours (i.e. being Protestant/Liberal) are
heritable
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