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Learning and Memory across the Lifespan

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Title: Learning and Memory across the Lifespan


1
Chapter 12
  • Learning and Memory across the Lifespan

2
12.1 Behavioral Processes
3
12.1 Behavioral Processes
  • The Developing Memory Infancy through
    Adolescence
  • Learning and Memory in Everyday Life Can
    Exposure to Classical Music Make Babies Smarter?
  • Sensitive Periods for Learning
  • The Aging Memory Adulthood through Old Age

4
Developing Memory in Infancy Some Learning Can
Occur Before Birth!
  • Gestational age (GA)time since conception.
  • By 25 weeks GA, enough development in fetuss
    brain and sense organs to perceive.
  • In studies (play sounds to human fetus)
  • Fetus (3436 weeks GA) moved in response to a
    sound habituated (reduced response) by trial 13.
  • Moved to 2nd stimulus habituated by trial 11.
  • Back to 1st stimulus habituated by trial 8.

5
Habituation to Sound (in 10 Human Fetuses)
Adapted from Hepper Shahidullah, 1992.
6
Time (sec.)
Polygraph recording of sucking on nipple
Figure adapted from Figure 1 of DeCasper
Spence, 1986.
Short pause
Long pause
Long pause
Unfamiliar story plays
Familiar story plays
Familiar story plays
Details of DeCasper Spence (1986)
paradigm Before birth, infants were played
familiar story in mothers voice memory for
story was tested after birth by playing
recordings of this story or unfamiliar story
while infants sucked on artificial nipple.
Infants tend to suck in bursts punctuated by
pauses (interburst intervals, IBIs). First,
researchers took baseline measurements of average
IBI. Then, conditioned some infants that long
IBIs would be reinforced with familiar story
while sucking short IBIs would be punished with
unfamiliar story while sucking. (Other infants
in counterbalanced conditioning, short intervals
were punished.)
7
Conditioning and Skill Learning in Young Children
  • Explosion of learning in first few years of life!
  • Most learning present in adults, present in
    infants.
  • But, perceptual and motor systems immature.
  • Until input/output systems mature, infants
    cannot fully learn or express.

8
Rovee-Collier Studies
  • (1993) Rovee-Collier studied instrumental
    conditioning in infants
  • 2-month-old infants learned to kick to move a
    colorful mobile (hung over the crib).
  • Illustrates instrumental conditioning.
  • With no reminders, Infants remembered foot-kick
    technique for 13 days.
  • With reminders, up to 21 weeks.

9
Rovee-Collier Studies
  • If crib liner with new pattern was used, babies
    didnt kick.
  • Illustrates context-dependent learning.

Courtesy of Carolyn Rovee-Collier
10
Infants and Classical Conditioning
  • Other studies show infants have basic components
    of classical conditioning.
  • Human and rat infants learned delay eyeblink
    conditioning.
  • But, use more trials than adults of their
    species.
  • Trace conditioning improved from infancy to
    early adulthood.
  • Shows that, with more mature development,
    organism can learn more efficiently (under
    increasingly difficult conditions).

11
Development of Episodic and Semantic Memory
  • Elicited imitationinfants ability to imitate an
    action at a later time.
  • From single observational learning training
    session.
  • In study, 10-month-olds are shown how to operate
    a toy puppet.
  • 4 months later, showed more interest in the
    puppet than control group (same age, no prior
    showing).
  • At 5 years, showed more interest and dexterity
    with the puppet than control group, though most
    could not recall previous exposure.

12
Development of Episodic and Semantic Memory
  • In study, 4-, 6-, and 8-year-olds taught 5 facts
    from an experimenter and 5 from a puppet.
  • One week later, 6- and 8-year-olds recalled and
    recognized more facts than 4-year-olds.
  • 6- and 8-year-olds had better recall of source,
    with more intra-experimental errors (i.e., knew
    it was learned in experiment, confused source).
  • 4-year-olds made more extra-experimental errors
    (i.e., thought learning was outside experiment,
    for example at school).

13
Episodic Memory in Children
Data from Drummey Newcombe, 2002.
14
Development of Working Memory
  • Working memory lifespan progression
  • English-speaking children 56 years can hold
    average digit span of 34 digits in working
    memory.
  • By 910 years, can hold 56 digits.
  • By 1415 years, can hold 7 digits (adult
    average).
  • Similar working memory progression seen with
    words and visual patterns.
  • Why fewer for children?
  • Lack of exposure.
  • Childrens performance improves with familiarity.

15
9
8
7
6
Girls
5
Mean Digits
Boys
4
3
2
1
0
5
6
7
8
9
10
11
12
13
14
15
Age (years)
Memory for digit span increases with age (reach
adult levels by about age 12 or 13) no
significant gender difference. Figure plotted
from data in Gardner, R. (1981). Digits forward
and digits backward as two separate tests
Normative data on 1567 school children. Journal
of Clinical Child Psychology, Summer 1981,
131135.
16
Learning and Memory in Everyday Life Can
Exposure to Classical Music Make Babies Smarter?
  • Limited intellectual benefits from exposure to
    classical music (no true Mozart effect).
  • Research shows little evidence that supports
    benefits zero evidence that the effect lasts
    longer than 1015 minutes.
  • So, why did scores increase?
  • Music may prime or prepare brain regions for
    abstract spatial reasoning or mental imagery.
  • Music may improve mood and subsequent
    performance.

17
Sensitive Periods for Learning
  • Sensitive periodstime ranges during which
    learning is enhanced or possible.
  • Examples
  • In male sparrows, 30100 days is a sensitive
    period for song learning.
  • In cats, 3 weeks to 60 days is a sensitive
    period for visual development.
  • But, for monkeys, all of the first 6 months are
    important for visual development.

18
Sensitive Periods for Learning
  • In study of 28 human infants who had cataract
    surgery at age 1 week to 9 months
  • ACUITY improved significantly over 1 month,
    with some improvement apparent after as little as
    1 hour of visual input.
  • Unlike older children, improvement was the same
    for eyes treated for monocular and binocular
    deprivation.
  • Visual input necessary for postnatal
    improvement its onset initiates rapid functional
    development.

19
Imprinting
  • Imprintingphenomenon in which some species
    (e.g., newborn goslings, turkeys, sheep, deer,
    buffalo) form a social bond with the first
    object they see.
  • Imprinting involves critical period for
    permanent change to occur.
  • http//www.youtube.com/watch?vLGBqQyZid04

Thomas D. McAvoy/ Time Magazine
20
Social Attachment Learning
  • Primates do not appear to imprint, but there is
    evidence of sensitive period for social
    attachment.
  • In study, Harry Harlow rears rhesus monkeys
    isolated from mothers in adolescence moved to
    group cages, show social retardation.
  • For rhesus monkeys, first months sensitive
    period for learning social interactions.
  • http//www.youtube.com/watch?vAn02zCsVEpY

21
Social Attachment Learning
  • Sensitive period for social attachment in humans?
    Consider children under Ceausescu regime (1970s)
  • Romanian children (RC) reared from infancy (up
    to 42 months) in depriving institutions, then
    placed in UK adoptive homes.
  • Compared with nondeprived UK-born children
    adopted before 6 months.
  • past
  • http//www.youtube.com/watch?vrXivHuugp3c
  • present
  • http//www.youtube.com/watch?vFWKQNMZa--Yfeature
    related

22
Social Attachment Learning
  • Findings
  • RC tested at time of entry to UK showed
    developmental impairment in cognitive function.
  • Tested again at 4 years all RC show
    improvement.
  • RC adopted before aged 6 months showed normal
    cognitive and social functioning.
  • But, RC adopted at 6 months or later still showed
    some cognitive deficits, mild social problems.
  • Suggests biological programming or neural
    damage from institutional deprivation varied
    outcomes related to early environmental
    stimulation.

23
A Sensitive Period in Humans
Data from Rutter et al., 1998.
24
Aging Memory Adulthood to Old Age
  • Working memory capacity is particularly
    vulnerable in old age.
  • Average STM capacity for digits drops from 7 (in
    early to middle adulthood) to 66.5 in elderly
    adults.

25
Conditioning and Skill Learning DeclineBut
Well-Learned Skills Survive
  • Learning decline begins around age 4050 in
    humans.
  • Also seen in elderly rabbits, rats, and cats.
  • However, well-established, highly practiced
    skills tend to be maintained or improved (chess
    and bridge experts).

26
Conditioning and Skill Learning DeclineBut
Well-Learned Skills Survive
  • In studies
  • Eyeblink conditioning may take twice as many
    trials in elderly.
  • Skill learning for rotary pursuit task and
    computer use take more time.

27
(B) Rotary pursuit skill learning
(A) Eyeblink classical conditioning
60
50
Mean distance covered
40
Trials to Criterion
30
20
10
0
18-29
30-39
40-49
50-59
60-69
70-70
Age (in years)
Age (in years)
Classical conditioning and skill learning decline
with aging.
(A) Plotted from data in Solomon et al., 1989,
Table 1. (B) From Kausler, D. (1994). Learning
and Memory in Normal Aging. New York Academic
Press, p. 38 fig 2.4 (top), which cites adapted
from Ruch, 1934.
28
Episodic and Semantic Memory Old Memories Fare
Better than New Learning
  • Healthy elderly adults tend to retain semantic
    knowledge, and recall many episodic memories.
  • In paired associates test
  • Elderly may be able to recognize words or
    images previously studied.
  • May have difficulty with recall.
  • May recall more information if given more time
    or allowed to self-pace rate of presentation.

29
Paired associate learning is impaired in elderly
adults relative to young adults when items are
presented at a rate of one every 1.5 seconds
impairment decreases if presentation rate is
slowed. Recall best when learning is self-paced,
though elderly subjects never quite reach same
performance as young subjects. From D. Kausler
(1994) Learning and Memory in Normal Aging, NY
Academic Press, p. 88, which cites adapted from
Canestrari, 1963, Table 2.
30
12.1 Interim Summary
  • Just about every kind of learning and memory
    observed in adults can also be observed in very
    young children.
  • Some simple kinds of learning (e.g.,
    habituation, recognition) can be observed before
    birth.
  • Other kinds of memory (particularly episodic
    and working memory) may be present at a very
    young age, but do not fully mature until late
    childhood or adolescence.

31
12.1 Interim Summary
  • Development of learning and memory abilities at
    least partially reflects brain development.
  • Sensitive periods time windows early in life
    when certain kinds of learning advance most
    rapidly.
  • Includes imprinting, social attachment learning.

32
12.1 Interim Summary
  • Many kinds of learning and memory show some
    decline in healthy aging.
  • Working memory is especially vulnerable.
  • In other memory domains (e.g., skills,
    conditioning, episodic and semantic memory) old,
    well-formed memories tend to survive well may be
    harder to acquire new memories.

33
12.2 Brain Substrates
34
12.2 Brain Substrates
  • The Genetic Basis of Learning and Memory
  • Neurons and Synapses in the Developing Brain
  • Gender Differences in Brain and Behavior
  • The Brain from Adulthood to Old Age

35
The Genetic Basis of Learning and Memory
  • DNAmaterial in cell nucleus instructions for
    replication.
  • Looks like twisted ladder sides sugar and
    phosphate molecules, rungs base pair.
  • Four kinds of DNA
  • Adenine
  • Thymine
  • Cytosine
  • Guanine

36
The Genetic Basis of Learning and Memory
  • DNA organized into chromosomes.
  • Humans have 23 chromosome pairs (one set from
    each parent).
  • 23rd pair determines gender.
  • XX female
  • XY male
  • Chromosomes subdivided into genes segment of DNA
    with information for building proteins from amino
    acids.
  • Probably 20,000 to 25,000 genes in humans.

37
Genes and DNA
CNRI/Photo Researchers, Inc.
38
Genetic Variation among Individuals Affects
Innate Learning Abilities
  • Mutationaccidental changes in DNA sequence.
  • Possibly from outside causes (e.g., radiation,
    viral infection) or copying error.
  • Mutations can
  • Be harmless.
  • Lead to cell malfunction, disease, death.
  • Be beneficial to the species.
  • New characteristics for reproduction or survival.

39
Genetic Variation among Individuals Affects
Innate Learning Abilities
  • Because of mutation over time, most genes have
    allelesnaturally occurring variations.
  • e.g., eye color

40
Genetic Variation among Individuals Affects
Innate Learning Abilities
  • Brain function also influenced by variations can
    affect learning and memory.
  • Examples
  • BDNF protein (the Val allele) may facilitate
    long-term plasticity.
  • Tyr allele (variant of His allele on 5-HT2AR
    gene) results in less-efficient serotonin
    receptors.
  • Perform slightly worse on delayed word recall
    task.

41
Genetic Influences on Learning and Memory in
Humans
(a) Data from Egan et al., 2003 (b) adapted from
de Quervain et al., 2003.
42
Selective Breeding and Twin Studies
  • Tryon (1940) Can animals be bred for learning
    ability?
  • Bred discrete groups of maze-bright and
    maze-dull rats in 7 generations.
  • By 7th generation, maze-bright offspring
    routinely out-perform rats bred from maze-dull
    line.

43
Data shown are hypothetical, based on Tryon, 1940.
44
Selective Breeding and Twin Studies
  • Multiple genes control characteristics of
    learning ability.
  • No single gene.
  • Human twin studies suggest that over half of the
    variation in memory scores may be genetic.
  • Identical twins have more similarity than
    fraternal.

45
The Influence of Environment
  • Rats raised in enriched environment (good
    sensory stimulation) have more dendrites and
    synapses.
  • Males had the most growth in visual cortex.
  • Female rats had the most growth in frontal
    cortex.

46
Neurons and Synapses in the Developing Brain
  • Neurons are overproduced, then weeded out.
  • Neurogenesis (neuron birth) most active during
    prenatal development continues to a limited
    degree throughout life.
  • Not uniform throughout brain some neurons form
    earlier than others.

47
Neurons and Synapses in the Developing Brain
  • In early development, glia guide cell migration
    produce molecules that modify growth of axons and
    dendrites.
  • Some glia (oligodendrocytes) produce myelin
    sheath, from birth to 18 years.
  • Neurotrophic factors (e.g., BDNF protein) help
    cells properly locate and specialize.
  • Without these chemical compounds, about 1/3 of
    neurons die (apoptosis), a natural phenomenon.

48
Neurons and Synapses in the Developing Brain
  • Synapses are also formed, then pruned.
  • Synaptogenesis (formation of new synapses)begins
    during gestation, but most active after birth to
    about age 6.
  • Tiny dendrite spines come and go if stimulated
    by neurotransmitters, synapses may form.
  • Unused synapses die (pruning).
  • New synapses may strengthen during non-REM
    sleep and unused may die during REM sleep.

49
Most synapses Occur on Dendritic Spines
(a) Adapted from Hof Morrison, 2004 (b)
adapted from Trachtenberg et al., 2002.
50
Sensitive Periods for Learning Reflect Sensitive
Periods for Neuronal Wiring
  • Neural pathways (and specific receptors) may
    develop rapidly during sensitive periods.
  • Apoptosis may then clean up neurons not used in
    in this sophisticated development.

51
The Promise of Stem Cells for Brain Repair
  • Young brains highly plastic older brains less
    able to adjust.
  • Can stem cells be integrated into adult brains?
  • Stem (especially from fetal tissue) cells have
    ability to develop into many cell types.
  • e.g, skin, liver, brain cells
  • Fetal stem cell transplant research still
    preliminary.
  • Tried in Parkinsons disease patients.
  • New neurons do not cure the underlying disease.

52
Embryonic Stem Cell Transplants in Brains of
Parkinsons Patients
Adapted from Freed et al., 2001.
53
Gender Differences in Brain and Behavior
  • In studies
  • Women often perform better than same-aged men
    on
  • List recall.
  • Story recall.
  • Memory for object location.
  • Men can outperform women in maze learning.
  • Men and women studied a fictitious town map
  • Men tended to learn a route more easily.
  • Women remembered more landmarks.

54
Gender Differences in Brain and Behavior
  • Male and female rats also show gender
    differences.
  • Sex hormones may contribute to gender-based
    learning differences.

55
Effects of Sex Hormones on Brain Organization
  • Pubertybodys physical change to sexual maturity
    in adolescence.
  • Surge in release of sex hormones.
  • Primarily estrogens in woman, androgens in men
    (especially testosterone).
  • In mammals and birds, testosterone surges in
    female fetuses and even more in male fetuses just
    before birth.

56
Effects of Sex Hormones on Brain Organization
  • During infancy, testosterone influences sex
    differences in brain development.
  • Larger in women
  • Lateral frontal cortex
  • Language areas (supramarginal gyrus)
  • Hippocampus
  • Larger in men
  • Visual and spatial processing areas

57
Effects of Sex Hormones on Adult Behavior
  • Gender differences in memory performance appear
    after puberty from circulating estrogen and
    testosterone.
  • Estrogen stimulates adult rats neuronal growth
    and synaptic plasticity (LTP), especially in the
    hippocampus.

58
Effects of Sex Hormones on Adult Behavior
  • Estrogen may increase verbal learning
    testosterone may increase spatial learning.
  • But, relationship between sex hormones
    (especially testosterone) and learning is
    complex.
  • Studies show male-to-female transsexual persons
    taking estrogen scored higher on paired-associate
    task.
  • Compared to similar group who had not yet
    started estrogen treatment.

59
Adulthood to Old Age Parts of the Aging Brain
Lose Neurons and Synapses
  • Slow human brain shrinkage, including the
    cerebellum, begins in young adulthood.
  • By age 80, average adult loses about 5 percent
    of brain weight.
  • Studies show
  • Cerebellum-dependent classical eyeblink
    conditioning slows with age.
  • However, there is little loss of hippocampal
    neurons in the healthy elderly.
  • Reductions in neurons disease warning signs.

60
Neuron Loss in Prefrontal Cortex of Aging Monkeys
Adapted from Smith et al., 2004.
61
Synaptic Connections May Be Less Stable in Old Age
  • Barnes (et. al.) suggest total number of neurons,
    synapses does NOT decrease rather, decrease in
    ability to maintain changes in synapse strength.
  • Rat and monkey studies suggest that synapses
    may be less stable in old age.
  • In studies, young rat and an old rat learned a
    figure 8-shaped maze. In second session,
    hippocampal LTP in the old rat was unstable.
  • Instability could contribute to spatial and
    episodic memory declines.

62
Hippocampal Neurons Encoding Location in Old and
Young Rats
(be) adapted from Barnes et al., 1997.
63
New Neurons for Old Brains? Adult Neurogenesis
  • Adult brain may be able to grow new neurons.
  • Adult neurogenesis has been studied (and
    reliably observed) in birds, fish, amphibians,
    reptiles.
  • Neurogenesis in mammals?
  • Studies show limited neurogenesis in brains of
    adults macaque monkeys and human cancer patients.
  • Most new neurons die within a few weeks.

64
12.2 Interim Summary
  • Development of learning and memory abilities at
    least partially reflects brain development.
  • Temporal and frontal cortex are among the last
    brain areas to fully mature.
  • May help explain why memory processes dependent
    on these areas are among last to reach full adult
    potency.

65
12.2 Interim Summary
  • Genes play a large role in determining learning
    and memory abilities.
  • Enriched environment studies show that
    experiences can also impact brain organization
    and an individuals abilities.
  • Before birth, the brain overproduces neurons and
    synapses.
  • Unnecessary neurons and synapses are gradually
    eliminated.

66
12.2 Interim Summary
  • Sensitive periods may reflect times when external
    inputs can easily and profoundly alter brain
    connectivity.
  • After sensitive period, large-scale
    organization of brain area in question may be
    fixed, and further learning (of the kind in
    question) may be limited to fine-tuning.

67
12.2 Interim Summary
  • Sex hormones, like estrogen and testosterone, can
    influence development and performance.
  • Leads to gender differences among adults in
    various kinds of learning and memory.
  • Influence on developing brain leads to gender
    differences even in very young individuals.

68
12.2 Interim Summary
  • Working memory declines in healthy aging.
  • Vulnerability may reflect normal frontal cortex
    shrinkage in healthy aging.
  • Pattern of memory loss in healthy aging may
    reflect loss of neurons and synapses.
  • Also, may reflect decrease in ability to
    maintain changes in synapse strength.
  • Thus, newly encoded information may be lost.

69
12.2 Interim Summary
  • New neurons produced throughout the lifespan.
  • But, particularly in humans, there is as yet
    little evidence that adult neurogenesis could
    provide large-scale replacement for damaged or
    aging neurons.

70
12.3 Clinical Perspectives
71
12.3 Clinical Perspectives
  • Down Syndrome
  • Alzheimers Disease
  • A Connection between Down Syndrome and
    Alzheimers Disease?
  • Unsolved MysteriesTreating (and Preventing)
    Alzheimers Disease

72
Down Syndrome
  • Down syndromecongenital form of mental
    retardation which occurs equally in girls and
    boys.
  • Retarded speech and language development low
    IQ scores.
  • Usually caused by trisomy 21 (extra copy of a
    chromosome 21).
  • During embryo formation, parents (usually
    mothers) chromosome fails to split properly.

Laura Dwight
73
Brain Abnormalities and Memory Impairments
  • In Down syndrome, brain size may be average at
    birth, but growth in some areas (e.g.,
    hippocampus, frontal cortex, cerebellum) may be
    stunted.
  • Individuals tend to have profound deficits in
    hippocampal-dependent memory abilities.
  • Young adults with Down syndrome performed at
    the 5-year-old level on mental abilities tasks.
  • Also, performed much worse on
    hippocampal-dependent memory tasks.

74
Hippocampal-DependentLearning and Down Syndrome
Data from Vicari, Bellucci, Carlesimo, 2000).
75
Brain Abnormalities and Specific Memory
Impairments in Down Syndrome
Figure summarizes performance on battery of tests
that require hippocampal function (like list
learning and spatial learning) compared with a
battery of tests that require prefrontal function
(like working memory). Adapted from Pennington
et al., 2003, Figure 2.
76
Animal Models of Down Syndrome
  • Mice bred for segmental trisomy (Ts65Dn mice)
    showed deficits in hippocampal-dependent tasks
    (e.g., location of maze goal).
  • Enriched environment improved spatial memory in
    female Ts65Dn mice.
  • Exacerbates impairment in Ts65Dn males.

77
Alzheimers Disease
  • Alzheimers Disease (AD)a form of progressive
    cognitive decline from accumulating brain
    deterioration.
  • AD affects about 4.5 million people in U.S.
  • As many as 50 percent of people over age 85 are
    afflicted.
  • http//www.youtube.com/watch?v7-P9lbTJ9Hw

78
Progressive Memory Loss and Cognitive
Deterioration
  • AD progression
  • Earliest symptoms of AD occur in episodic
    memory, such as forgetting recent visitors.
  • Later, there are declines in semantic memory
    (e.g., forgetting familiar names, locations).
  • Next, conditioning and skill memory
    deteriorate.
  • In late-stage AD, there is often a lack of
    awareness and daily living skills.
  • http//www.youtube.com/watch?voTEbq4h-kvQ

79
Patients with AD show marked impairment in many
forms of memory, including list learning. Over
three trials with a 10-word list, AD patients
recall fewer items than same-aged healthy
controls after a 10 minute delay, the patients
recall almost none of the studied words. Adapted
from Figure 1 of Moulin et al. (2004).
80
Plaques and Tangles in the Brain
  • Amyloid plaques deposits of beta-amyloid
    (abnormal byproduct of amyloid precursor protein,
    or APP kills adjacent neurons).
  • Plaques are fairly evenly distributed across
    cerebral cortex.
  • Neurofibrillary tangles collapsed protein
    scaffolding within neurons.
  • Early in AD, accumulate in hippocampus and MTL,
    relating to semantic and episodic memory
    deficits.
  • Hippocampal shrinkage early AD warning sign.

81
Plaques and TanglesHallmarks of Alzheimers
Disease
a) Amyloid plaque (dark center spot) surrounded
by residue of degenerating cells.
b) Neurofibrillary tangles (seen as darkened
areas).
(a) Cecil Fox/Science Source/ Photo Researchers.
(b) Adapted from Figure 3 of Hardy Gwinn-Hardy,
1998.
82
Plaques and Tangles in the Brain
  • Verification of presence of plaques and tangles
    (to confirm AD diagnosis) can only happen at
    autopsy.
  • 10 to 20 percent of probable AD diagnoses
    (based on MRI, PET, lumbar puncture, etc.) are
    incorrect.
  • Many other conditions (some treatable) mimic
    AD, so better diagnostic test needed.
  • e.g., vitamin B deficiency, hypothyroidism,
    depression

83
Genetic Basis of Alzheimers Disease
  • Several genes implicated in AD.
  • Most progress understanding genetic cause of
    early-onset AD (begins at 3550 years).
  • Less than 1 percent of AD cases early-onset.
  • Caused by genetic mutations, which are
    autosomal dominant (meaning, just one mutated
    gene from either parent will trigger early-onset
    AD).

84
Connection Between Down Syndrome and Alzheimers
Disease?
  • Chromosome 21 (implicated in Down syndrome)
    contains APP (implicated in AD).
  • By age 3540, adults with Down syndrome develop
    neural plaques and tangles.
  • Half of Down syndrome patients show memory
    decline and other symptoms of AD other half do
    NOT show cognitive decline.
  • Why? Unclear. Explanation will help in
    understanding both pathologies.

85
Unsolved MysteriesTreating (and Preventing)
Alzheimers Disease
  • Cholinesterase inhibitors treat forgetfulness and
    anxiety.
  • Inhibiting breakdown of neurotransmitter
    acetylcholine (depleted in patients with AD).
  • Memantine blocks glutamate receptors.
  • May help protect neurons from
    glutamate-mediated damage, slow cognitive decline.

86
Unsolved MysteriesTreating (and Preventing)
Alzheimers Disease
  • Risk factors for AD include
  • Type-II diabetes
  • High LDL (bad cholesterol)
  • Previous head injury
  • Stroke
  • High blood pressure
  • High levels of cognitive activity may slow AD
    symptoms.

87
12.3 Interim Summary
  • Down syndrome condition in babies born with
    extra copy of chromosome 21.
  • Children with Down syndrome have cognitive
    impairments.
  • Includes memory impairments.
  • Some brain areas tend to be abnormally small.
  • Includes hippocampus, frontal cortex,
    cerebellum.

88
12.3 Interim Summary
  • In Alzheimers disease, plaques and tangles
    accumulate in the brain.
  • Memory symptoms are prominent early in the
    disease.
  • Consistent with finding that hippocampus and
    nearby MTL areas suffer pathology early in
    disease.
  • Several genes may contribute to an individuals
    risk for the common, late-onset form of the
    disease.
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