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Chapter Outline and Key Terms for Chapter 13
I. The Nature of Intelligence
a. What does “intelligence” mean?
i. Intelligence is the ability to reason, to understand, and to profit from experience.
ii. Typically expressed as the intelligence quotient (IQ), averaging 100 points.
1. Tests are criticized for emphasizing academic “smarts” and biased questions.
2. Positively correlated to income, socioeconomic level.
3. Negatively correlated to juvenile delinquency.
b. The structure of intelligence
i. Debate whether intelligence is a single capability (lumpers) or a collection of several
abilities (splitters).
II. Biological Origins of Intelligence
a. The brain and intelligence
i. Einstein had larger parietal lobes, and other researchers suggest that an active,
distributed network is present in “intelligent” individuals.
b. Brain size (relative to body size) is somewhat correlated to intelligence.
i. Other possible correlates are smaller cortical columns and greater frontal gray matter.
c. IQ scores are correlated with processing efficiency.
i. Higher nerve conduction and processing speed correlated with faster cognitive speed.
ii. Higher myelination increases speed and reduces “cross talk” to adjacent areas.
iii. Reduced energy use.
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iv. Greater cortical inter-connectivity.
d. Specific abilities and the brain
i. Linguistic Left frontal and temporal lobes.
ii. Logical-mathematical Left prefrontal cortex (rote calculation) and parietal cortices
(active calculation).
iii. Spatial Somatosensory and visual functions with right parietal structures.
e. Heredity and environment
i. Heritability of intelligence
1. About 50% and increases with age; identical twins reared apart are more similar
than fraternal twins reared together.
2. Greater cognitive performance linked to genes for brain size (ASPM).
3. Greater heritability for general than specific abilities.
4. Neurogenesis and signaling gene (PACAP) also implicated.
5. Likely many different genes contribute.
ii. The genetic controversy
1. Whether ethnic differences in intelligence are genetic.
2. Identical twins raised apart have more similar IQ scores than adopted
environments.
3. However, some IQ tests are culturally biased towards certain groups.
iii. Environmental effects
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1. Socioeconomic level and parental education related to intelligence of children, but
genetic similarity confounds analysis.
2. Prenatal pesticide exposure associated with cognitive deficits.
3. Level of infectious disease best predictor of national differences in intelligence, as
the energy needed to fight off disease decreases brain development.
4. Electrical stimulation of prefrontal cortex and working memory training tasks also
improve performance.
III. Deficiencies and Disorders of Intelligence
a. Effects of aging on intelligence
i. Perceptual speed dropped after the age of 25, and numeric memory at 60.
ii. Default mode network, which encompasses portions of the parietal, frontal and
temporal lobes, is responsible for preparedness for action.
iii. Nonphysical causes such as lack of skill practice, low self-esteem, and poor diet can
decrease intelligence.
iv. Sex hormones can provide protection against the cognitive effects of aging, especially
estrogen and testosterone (for spatial memory in men).
b. Intellectual disability
i. Intellectual disability IQ of less than 70 and inability to live independently.
ii. Down syndrome, caused by having three chromosome 21’s, results in IQ values in
the 40-55 range and occurs in 1 of every 700 births.
iii. Fragile X syndrome due to mutation in fragile X mental retardation 1 gene (FMR1),
where CGG nucleotide repeats exceed 45.
iv. Phenylketonuria (PKU) is due to an inherited inability to metabolize phenylalanine.
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v. Hydrocephalus is due to cerebrospinal fluid buildup in the ventricles.
c. Autism spectrum disorder
i. Autism Spectrum Disorder (ASD) includes social deficits, communication
difficulties and repetitive behaviors.
ii. Cognitive and social impairment
1. Impaired in communication, imagination and socialization.
2. Autistics are hypothesized to lack a theory of mind, the ability to infer what other
people are thinking based on experience.
3. Empathy may come from mirror neurons, which may be deficient in ASD
individuals.
iii. Brain anomalies
1. Occurs early, during brain development, and includes the brain stem, cerebellum
and temporal lobes.
2. Lack of coordination between amygdala and ventromedial prefrontal cortex,
preventing ASD individuals from looking at faces, as well as tracking objects in
space.
3. Decreased white matter in adults causes loss of synchronized activity.
4. Biochemical anomalies include abnormal serotonin, glutamate, GABA, and
oxytocin levels.
iv. The environment
1. Disrupted brain development due to high levels of traffic pollution.
2. Maternal metabolic conditions such as obesity, diabetes, and hypertension also
linked to ASD, though folic acid supplements reduce risks.
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v. Heredity
1. Siblings of ASD children are 25 times more likely to develop the disorder than the
general population.
2. ASD genes expressed in superficial cortex, interfering with connections between
layers and hemispheres.
3. Absence of genes in frontal and temporal cortices of ASD individuals indicate a
possible epigenetic influence.
4. ASD is two times more common in boys.
vi. Autistic savants and high-functioning ASD individuals
1. An autistic savant is a person with one or more exceptional skills but whose
overall functioning is below normal.
2. High-functioning individuals with ASD have a limited impairment that can be
overcome with effort, like Temple Grandin.
3. The source of the skill is unknown but may arise when executive or integrative
function within the brain is compromised.
d. Attention deficit hyperactivity disorder
i. ADHD is characterized by impulsiveness, inability to sustain attention, learning
difficulty and hyperactivity, which persists into adulthood in many cases.
ii. Brain anomalies in ADHD
1. Multiple areas implicated included prefrontal cortex, cerebellum, and right
caudate nucleus of the striatum (reduced in size).
2. ADHD may result from disruption of the attention-inhibition network of the
temporal and inferior parietal areas.
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iii. Genes, neurotransmitters, and ADHD
1. ADHD is 56 times more prevalent in relatives than non-relatives; concordance
up to 83% in identical twins and 47% in fraternal twins.
2. Genes involved in cell migration, synaptic excitability, and neuronal plasticity.
3. Additional implicated genes related to synaptic functioning, neural development
and survival, and learning.
4. Various neurotransmitters, including dopamine, norepinephrine, and serotonin
e.g., reduced activity in dopamine pathways and impaired reward.
5. Ritalin (a stimulant) increases norepinephrine output to the prefrontal cortex and
improves impulse control, working memory, and learning.
iv. The environment and ADHD
1. ADHD incidence is increased by maternal stress, smoking, and drug abuse during
pregnancy.
2. Increased prevalence with lead and pesticide exposure.

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