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Chapter 12
Learning and
Memory across
the Lifespan
12.1
Behavioral
Processes
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
3
Developing Memory in Infancy: Some
Learning Can Occur Before Birth!
•
Gestational age (GA)—time since
conception.
•
By 25 weeks GA, enough development in
fetus’s brain and sense organs to perceive.
•
In studies (play sounds to human fetus):
Fetus (34–36 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.
4
Habituation to Sound
(in 10 Human Fetuses)
Adapted from Hepper & Shahidullah, 1992.
5
Polygraph
recording of
sucking on
nipple
Short
pause
Unfamiliar
story
plays
Long
pause
Long
pause
Familiar
story
plays
Familiar
story
plays
Figure adapted from Figure 1 of DeCasper & Spence, 1986.
Time
(sec.)
Details of DeCasper & Spence (1986) paradigm:
Before birth, infants were played familiar story in mother’s 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.)
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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.
7
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 1–3 days.
With reminders, up to 21 weeks.
8
Rovee-Collier Studies
If crib liner with new pattern was used,
babies didn’t kick.
Illustrates context-dependent
learning.
Courtesy of Carolyn Rovee-Collier
•
9
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).
10
Development of Episodic and
Semantic Memory
•
Elicited imitation—infants’ 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.
11
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).
12
Episodic Memory in Children
Data from Drummey & Newcombe, 2002.
13
Development of
Working Memory
•
Working memory lifespan progression:
English-speaking children 5–6 years can hold
average digit span of 3–4 digits in working memory.
By 9–10 years, can hold 5–6 digits.
By 14–15 years, can hold 7 digits (adult average).
Similar working memory progression seen with
words and visual patterns.
•
Why fewer for children?
Lack of exposure.
Children’s performance improves with familiarity.
14
9
8
Mean Digits
7
6
Girls
Boys
5
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, 131–135.
15
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 10–15 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.
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Sensitive Periods for Learning
•
Sensitive periods—time ranges during
which learning is enhanced or possible.
•
Examples:
In male sparrows, 30–100 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.
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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.
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Imprinting
•
Imprinting—phenomenon
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?v=LGBqQyZid04
Thomas D. McAvoy/ Time Magazine
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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?v=An02zCsVEpY
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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?v=rXivHuugp3c
present
http://www.youtube.com/watch?v=FWKQNMZa--Y&feature=related
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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.
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A Sensitive Period in Humans
Data from Rutter et al., 1998.
23
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 6–6.5 in
elderly adults.
24
Conditioning and Skill Learning
Decline—But Well-Learned Skills Survive
•
Learning decline begins around age 40–50
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).
25
Conditioning and Skill Learning
Decline—But 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.
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60
Trials to Criterion
(B) Rotary pursuit skill learning
Mean distance covered
(A) Eyeblink classical conditioning
50
40
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.
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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.
28
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.
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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.
30
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.
31
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.
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12.2
Brain
Substrates
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
34
The Genetic Basis of Learning
and Memory
•
DNA—material 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
35
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.
36
37
CNRI/Photo Researchers, Inc.
Genes
and DNA
Genetic Variation among Individuals
Affects Innate Learning Abilities
•
Mutation—accidental 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.
38
Genetic Variation among Individuals
Affects Innate Learning Abilities
•
Because of mutation over time, most genes
have alleles—naturally occurring variations.
e.g., eye color
Bey2: blue-blue
Bey2: BROWNblue
Bey2: BROWNblue
Bey2: BROWNblue
Bey2: blueblue
Bey2: blueblue
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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 longterm 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.
40
Genetic Influences on
Learning and Memory in Humans
(a) Data from Egan et al., 2003; (b) adapted from de Quervain et al., 2003.
41
Selective Breeding and
Twin Studies
•
Tryon (1940): Can animals be bred for
learning ability?
Bred discrete groups of maze-bright and mazedull rats in 7 generations.
By 7th generation, maze-bright offspring routinely
out-perform rats bred from maze-dull line.
42
Data shown are hypothetical, based on Tryon, 1940.
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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.
44
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.
45
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.
46
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.
47
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.
48
Most synapses Occur on Dendritic Spines
(a) Adapted from Hof & Morrison, 2004; (b) adapted from Trachtenberg et al., 2002.
49
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.
50
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 Parkinson’s disease patients.
New neurons do not cure the underlying disease.
51
Embryonic Stem Cell Transplants in
Brains of Parkinson’s Patients
Adapted from Freed et al., 2001.
52
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.
53
Gender Differences in
Brain and Behavior
•
Male and female rats also show gender
differences.
•
Sex hormones may contribute to genderbased learning differences.
54
Effects of Sex Hormones on
Brain Organization
•
Puberty—body’s 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.
55
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
56
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.
57
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.
58
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.
59
Neuron Loss in Prefrontal Cortex
of Aging Monkeys
Adapted from Smith et al., 2004.
60
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.
61
Hippocampal Neurons Encoding
Location in Old and Young Rats
(b–e) adapted from Barnes et al., 1997.
62
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.
63
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.
64
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 individual’s abilities.
•
Before birth, the brain overproduces
neurons and synapses.
Unnecessary neurons and synapses are
gradually eliminated.
65
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.
66
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.
67
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.
68
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.
69
12.3
Clinical
Perspectives
12.3 Clinical Perspectives
•
Down Syndrome
•
Alzheimer’s Disease
•
A Connection between Down Syndrome
and Alzheimer’s Disease?
•
Unsolved Mysteries—Treating (and
Preventing) Alzheimer’s Disease
71
Down Syndrome
Down syndrome—congenital
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).
Laura Dwight
•
During embryo formation, parent’s (usually mother’s)
chromosome fails to split properly.
72
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 hippocampaldependent memory tasks.
73
Hippocampal-Dependent
Learning and Down Syndrome
Data from Vicari, Bellucci, & Carlesimo, 2000).
74
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.
75
Animal Models of Down
Syndrome
•
Mice bred for segmental trisomy (Ts65Dn
mice) showed deficits in hippocampaldependent tasks (e.g., location of maze goal).
•
Enriched environment improved spatial
memory in female Ts65Dn mice.
Exacerbates impairment in Ts65Dn males.
76
Alzheimer’s Disease
•
Alzheimer’s 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?v=7-P9lbTJ9Hw
77
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?v=oTEbq4h-kvQ
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10
Words Recalled
8
Healthy
Elderly
6
4
2
Early AD
0
1
2
3
Delay
Trial
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).
79
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.
80
Plaques and Tangles—
Hallmarks of Alzheimer’s 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.
81
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
82
Genetic Basis of
Alzheimer’s Disease
•
Several genes implicated in AD.
•
Most progress understanding genetic cause
of early-onset AD (begins at 35–50 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).
83
Connection Between Down
Syndrome and Alzheimer’s Disease?
•
Chromosome 21 (implicated in Down
syndrome) contains APP (implicated in AD).
•
By age 35–40, 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.
84
Unsolved Mysteries—Treating (and
Preventing) Alzheimer’s 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 glutamatemediated damage, slow cognitive decline.
85
Unsolved Mysteries—Treating (and
Preventing) Alzheimer’s 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.
86
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.
87
12.3 Interim Summary
•
In Alzheimer’s 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
individual’s risk for the common, late-onset
form of the disease.
88