251 Unit 10.1 fa24
MEMORY
DEVELOPMENT
AND AGING
Unit 10, Part 1: Behavioral
Processes of Memory
Development
PSYC 251
Learning and Memory
Fall 2024 Session 38
Wednesday, December 4
Copyright © 2024 Eric W. Gobel, PhD
251 Unit 10.1 fa24
Memory Development and Aging
• Behavioral processes
• The developing memory: Prenatal, infancy, and childhood
• Sensitive periods for early learning
• Adolescence: Crossing from childhood into adulthood
• The aging memory: Adulthood through old age
• Brain substrates
• Clinical perspectives
251 Unit 10.1 fa24
Memory Development and Aging
• Memory systems development parallels development of
their underlying brain substrates
• Understanding development of learning & memory systems:
• Helps tailor school and teaching to place appropriate demands on
students.
• Helps us understand normal brain development and opens possibilities
for extending/improving function across the life span.
• One caveat:
• Developmental trends represent averages across considerable
variability.
• Variability exists within a cohort (e.g., the huge diversity of ACT scores
for high school seniors) and across developmental trajectories.
251 Unit 10.1A fa24
Memory Development and Aging
• Behavioral processes
• The developing memory: Prenatal, infancy, and childhood
• Sensitive periods for early learning
• Adolescence: Crossing from childhood into adulthood
• The aging memory: Adulthood through old age
• Brain substrates
• Clinical perspectives
251 Unit 10.1A fa24
Memory Development: Infancy to Childhood
• Incredibly, the ability to learn is intact even before birth.
• By 34-36 weeks, auditory habituation:
• A speaker is placed on the mother’s abdomen.
• Sounds initially cause fetal movement.
• Repeated sounds decrease responses.
251 Unit 10.1A fa24
Memory Development: Infancy to Childhood
• Immediately after birth, human infants demonstrate incredible
learning abilities:
• Language
• Motor control
• Social skills
• Some limitations are evident due to immature sensory and
motor systems.
• Formal experiments show excellent operant and classical
conditioning…
https://www.youtube.com/watch?v=ZgOu_Uc00ao (3:18)
251 Unit 10.1A fa24
Rovee-Collier Infant Mobile Studies
251 Unit 10.1A fa24
Memory Development: Infancy to Childhood
• Infant operant conditioning:
kick leg → move mobile
• Quickly leads to vigorous leg
kicking
• Memory maintained for days
(no reminders) to weeks (with
reminders)
• Discriminant stimuli:
• Trained in crib with striped crib liner
• Kicking in striped cribs
• No kicking in plain cribs
251 Unit 10.1A fa24
Memory Development: Infancy to Childhood
• Infants also show classical conditioning (remember baby
Little Albert?)
• Basics intact from birth, some aspects mature:
• Eye-blink conditioning slower in infants than adults
• Trace conditioning (gap between CS and US) not possible until age 4,
and even then, still a bit slower than adults
251 Unit 10.1A fa24
Memory Development: Infancy to Childhood
How about infant declarative memory systems?
• Infants have semantic memory, which develops
further over time.
• The development of episodic memory is less clear.
• Let’s look at each of these in turn…
251 Unit 10.1A fa24
Memory Development: Infancy to Childhood
• Infants have semantic memory, which develops
further over time.
• Elicited imitation paradigm:
• 10-month-old children shown a) how to operate a toy puppet or b) the
puppet alone (no demonstration)
• Four months later, presented with same puppet
• Children who had seen the puppet demonstrated were later more
interested in it and were better able to use it.
• Shows intact recognition for puppet and how to operate it!
• Episodic memory?
251 Unit 10.1A fa24
Memory Development: Infancy to Childhood
• Episodic memory seems to develop more slowly.
• Children hid stuffed toys around their homes and were later tested for
the what, where, and when of these events.
• 3-year-olds were worse than 4-year-olds at episodic memory retrieval
251 Unit 10.1A fa24
Memory Development: Infancy to Childhood
• Episodic memory seems to develop more slowly.
• Children hid stuffed toys around their homes and were later tested for
the what, where, and when of these events.
• 3-year-olds were worse than 4-year-olds at episodic memory retrieval
• Do you remember your early childhood? Why not?
• Possible causes of infantile amnesia:
• Slow hippocampus development; needed to support episodic memory
formation?
• Developing sense of self? Infants don’t pass the “red mark” test until
about 24 months.
• Performance issue? Infants may have episodic memories, but it’s hard
for them to express these memories.
• The correct explanation is still unclear.
251 Unit 10.1A fa24
Memory Development: Infancy to Childhood
• Source memory seems to develop even more slowly.
• Children learned factual question-answer pairs and were later tested for
source memory.
• Young children had poor source memory and could rarely recall having
learned the pair within the experiment.
• Why?
251 Unit 10.1B fa24
Memory Development and Aging
• Behavioral processes
• The developing memory: Prenatal, infancy, and childhood
• Sensitive periods for early learning
• Adolescence: Crossing from childhood into adulthood
• The aging memory: Adulthood through old age
• Brain substrates
• Clinical perspectives
251 Unit 10.1B fa24
Sensitive Periods for Early Learning
• Some learning abilities are only available early in life, a so-
called sensitive period or critical period after which some
forms of learning may become difficult/impossible.
• Imprinting: forming a close bond
with first individual seen after birth.
• Common in birds, but also occurs in other
species.
• Bond forms best immediately after birth;
after this critical period, harder to form.
https://www.youtube.com/watch?v=eqZmW7uIPW4
251 Unit 10.1B fa24
Critical Period for Imprinting: Lorenz
251 Unit 10.1B fa24
Sensitive Periods for Early Learning
• Some learning abilities are only available early in life, a so-
called sensitive period or critical period after which some
forms of learning may become difficult/impossible.
• Sensitive/critical periods are also evident in other systems:
• Visual development: impaired visual input early in development leads
to permanent disruption of visual system.
• Male sparrows raised in isolation don’t develop normal songs, unless
played tape recordings during the exact right developmental time frame
(30-100 days after birth).
• Human language has also suggested to have a sensitive
period. Let’s take a closer look…
http://www.youtube.com/watch?v=QzkMo45pcUo
251 Unit 10.1B fa24
Sensitive Period for Visual Development
251 Unit 10.1B fa24
Sensitive Periods for Early Learning
• Sensitive/critical periods for language learning?
• Skill at phonetic discriminations for sound distinctions not
used in exposed languages is lost during early development.
251 Unit 10.1B fa24
Sensitive Periods for Early Learning
• Sensitive/critical periods for language learning?
• Skill at phonetic discriminations for sound distinctions not
used in exposed languages is lost during early development.
• Some evidence suggests language must be learned before
~12 years of age to be fully mastered.
• Despite extensive tutoring, “feral children” fail to develop normal
language (e.g., Genie).
• On the other hand…
• Adults can learn a second language more quickly than young children,
though they don’t usually end up with the same level of mastery.
• Differences in mastery may be more related to time-on-task, which
young children have lots of relative to most adults.
251 Unit 10.1C fa24
Memory Development and Aging
• Behavioral processes
• The developing memory: Prenatal, infancy, and childhood
• Sensitive periods for early learning
• Adolescence: Crossing from childhood into adulthood
• The aging memory: Adulthood through old age
• Brain substrates
• Clinical perspectives
251 Unit 10.1C fa24
Adolescence: Childhood to Adulthood
• Adolescence: the transitional stage between the onset of
puberty and full adulthood.
• Strong development of working memory and central
executive function during adolescence.
• Digit span increases through early teens.
• Executive function develops throughout early adulthood.
• Why?
251 Unit 10.1C fa24
Adolescence: Childhood to Adulthood
• Adolescence: the transitional stage between the onset of
puberty and full adulthood.
• Strong development of working memory and central
executive function during adolescence.
• Ongoing development of frontal lobes
• Increasing familiarity leading to better WM encoding (e.g., chunking)
• Child chess experts can remember more locations of chess pieces than non-
chess-playing adults, due to higher familiarity.
251 Unit 10.1C fa24
Adolescence: Childhood to Adulthood
• Adolescence: the transitional stage between the onset of
puberty and full adulthood.
• Strong development of working memory and central
executive function during adolescence.
• Gender differences also emerge during this time:
• Women perform slightly better (on average) on verbal memory and on
spatial learning of landmark locations.
• Men perform slightly better (on average) on spatial learning of routes.
• Similar gender differences evident in many mammals, suggesting the
differences aren’t purely cultural.
• Gender differences may be due partly to different levels of sex
hormones between males and females (more on this later).
251 Unit 10.1D fa24
Memory Development and Aging
• Behavioral processes
• The developing memory: Prenatal, infancy, and childhood
• Sensitive periods for early learning
• Adolescence: Crossing from childhood into adulthood
• The aging memory: Adulthood through old age
• Brain substrates
• Clinical perspectives
251 Unit 10.1D fa24
Aging Memory: Adulthood to Old Age
• Adult abilities can remain stable for many years.
• Unfortunately, though, the overall pattern in old age is decline
in most basic learning, memory, and cognitive skills.
251 Unit 10.1D fa24
Aging Memory: Adulthood to Old Age
• Adult abilities can remain stable for many years.
• Unfortunately, though, the overall pattern in old age is decline
in most basic learning, memory, and cognitive skills.
• Working memory is one of the first to show age-related
decline.
• Proactive interference? Older adults have learned much more and may
be less able to prevent this from interfering with the contents of working
memory.
• Similar trends for conditioning and skill learning:
• Eyeblink conditioning starts declining at 40-50 years and can take
twice as long in older adults relative to young adults.
• Skill learning declines rapidly after 60 years (e.g., rotary pursuit).
251 Unit 10.1D fa24
Aging Memory: Adulthood to Old Age
• Semantic and episodic memory show uneven decline:
• Ability to retain and retrieve these memories shows little
decline during healthy aging.
• e.g., older adults who studied Spanish in high school still recalled many
Spanish words learned, even with little practice over long spans of time.
• Unfortunately, the ability to encode episodic and semantic
memories (i.e., encoding) does decline with age.
• Older adults show poor paired associate learning.
• Deficits can be ameliorated with slower rates of presentation and/or
meaningful stimuli.
251 Unit 10.1D fa24
Aging Memory: Adulthood to Old Age
• Some good news: strong compensation
• Although basic skills decline, older adults have more skills and
experience to draw on.
• This richer pool of experience can often help compensate for
diminished skills and enable performance of complex skills at the same
or better level than in young adults!
• Example: older typists make slower movements but have better
semantic memory and need to look at their manuscript less often,
leading to excellent overall performance.
• Warning: use it or lose it!
• Overall performance is only preserved in skills that are practiced
throughout aging.
251 Unit 10.1 fa24
Interim Summary: Behavioral Processes
• Learning and memory ability varies over the life span.
• In infancy:
• Habituation, instrumental conditioning, and classical conditioning are
intact (though developing) from birth or earlier.
• Semantic memory seems intact (but developing) from an early age, but
episodic memory may take more time to fully develop.
• During adolescence, strong development of working memory and
executive function, and the appearance of small gender
differences.
• Through adulthood, period of stability but overall decline in most
basic memory and cognitive skills, especially working memory.
• Storage & retrieval of declarative memories is strong throughout healthy
aging, but formation of new declarative and skill memories declines.
• Some learning exhibits sensitive periods (such as imprinting), but
evidence for a sensitive period for language is unclear.
251 Unit 10.3B fa24
MEMORY
DEVELOPMENT
AND AGING
Finish Part 1: Behavior
Part 2: Alzheimer’s Disease
PSYC 251
Learning and Memory
Fall 2024 Session 39
Friday, December 6
Copyright © 2024 Eric W. Gobel, PhD
251 Unit 10.3B fa24
Memory Development and Aging
• Behavioral processes
• Brain substrates
• Clinical perspectives
• Down syndrome
• Alzheimer’s disease
• A connection between Down syndrome and Alzheimer’s disease
251 Unit 10.3B fa24
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 the U.S.
• As many as 50% of people over age 85 are afflicted.
• Progression of memory loss in Alzheimer’s disease:
• Earliest symptoms are episodic memory failures, such as forgetting
recent visitors.
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251 Unit 10.3B fa24
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 3 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).
251 Unit 10.3B fa24
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 the U.S.
• As many as 50% of people over age 85 are afflicted.
• Progression of memory loss in Alzheimer’s disease:
• Earliest symptoms are episodic memory failures, such as forgetting
recent visitors.
• Later, there are declines in semantic memory (e.g., forgetting familiar
names, locations).
• Much later, conditioning and skill memory deteriorate.
• In late-stage AD, there is often a lack of awareness and activities of
daily living (ADL) skills.
115
251 Unit 10.3B fa24
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 tau protein, which normally
functions as scaffolding within neurons.
• Early in AD, accumulate in hippocampus and MTL, relating to declarative
memory deficits (episodic and semantic).
• Hippocampal shrinkage = early AD warning sign
• Verification of presence of plaques and tangles (to confirm AD
diagnosis) can only happen at autopsy.
• 10% to 20% of “probable AD” diagnoses (based on MRI, PET, lumbar
puncture, etc.) are incorrect.
• Many other conditions (some treatable) mimic AD (e.g., vitamin B
deficiency, hypothyroidism, depression)
• So better diagnostic tests needed (e.g., PiB imaging on next slide)
119
251 Unit 10.3B fa24
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.
251 Unit 10.3B fa24
251 Unit 10.3B fa24
251 Unit 10.3B fa24
Genetic Basis of Alzheimer’s Disease
• Several genes are implicated in AD.
• Most progress is in understanding genetic cause of early-
onset Alzheimer’s disease (begins at 35–50 years).
• Early-onset = less than 1% of AD cases
• Caused by genetic mutations that are autosomal dominant (just one
mutated gene from either parent will likely trigger early-onset AD).
122
251 Unit 10.3B fa24
Possible Causes of Alzheimer’s Disease
• Early-onset Alzheimer’s disease (onset < 60 years; rare =
less than 1% of cases) has significant genetic component
• Autosomal dominant mutations found in genes coding for proteins
involved in amyloid processing are linked to early-onset AD
• Amyloid precursor protein (APP), presenilin (PS1, PS2) mutations
• Late-onset Alzheimer’s disease (onset > 60 years; 99% of
cases) is more influenced by environmental factors
• But also linked to ApoE4 mutation of gene for apolipoprotein E
• Neurobiological research approach: Study AD-linked
mutations to learn about mechanisms of neuropathology
• These mutations cause β-amyloid protein to accumulate and
cluster into plaques
251 Unit 10.3B fa24
Treatment and Prevention of Alzheimer’s
• Cholinergic agonists
• ACh has widespread cortical
and hippocampal projections
• AChE inhibitors (e.g., Aricept)
• Methods to decrease β-amyloid accumulation
• Aβ1-42 vaccine
Leqembi (new AD drug)
• Antioxidants
• Prevention: remain active cognitively, socially, physically
• Promotes neuronal survival and hippocampal neurogenesis
• Slows cognitive aging in both healthy and disease states
251 Unit 10.3B fa24
Interim Summary: Clinical Perspectives
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 the disease.
• Several genes may contribute to an individual’s risk for the
common, late-onset form of the disease.
125
251 Unit 10.3B fa24
The brain-changing benefits of exercise
(Wendy Suzuki, NYU)
https://www.ted.com/talks/wendy_suzuki_the_brain_changing_benefits_of_exercise
On YouTube: https://www.youtube.com/watch?v=BHY0FxzoKZE
Longer talk: https://www.youtube.com/watch?v=Y0cI6uxSnuc
251 Unit 10 fa24
Interested in Memory Development & AD?
If you are interested in learning more about the behavioral and
neural aspects of memory development:
• PSYC 273 Developmental Psychology (multiple sections
every semester)
• PSYC 350 Developmental Cognitive Neuroscience (taught
in spring by Dr. Guy)
If you are interested in learning more the clinical implications of
memory development and aging such as Alzheimer's Disease:
• BIOL 357 Neural Disease, Degeneration, and Regeneration
covers neurodegenerative diseases (including Alzheimer’s and
Parkinson’s) in even more depth (taught in fall/spring by Dr. Yu)
• Pre-requisites: BIOL 251, BIOL 282, NEUR 101
251 Unit 10 fa24
In-Class Reflection Question:
Metacognitive Self-Reflection
After self-reflection, answer some or all of these question
prompts on Top Hat:
• What did you learn in this course? It may help to identify
the three most important skills/concepts that you learned
and/or experiences that you had in the course.
• How have your ideas, perspectives, attitudes, and skills
changed as a result of this course?
• How will you apply the concepts and skills learned in this
course in the future?