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Neurocognitive Aging
Katherine M. Krpan
PSY 393
March 27th, 2007
1
Outline

The Healthy Aging Brain
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What declines and what doesn't
Theories on neurocognitive aging
Laterality in the aging brain
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Disorders of the Aging Brain
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Dementias
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Dedifferentiation and Compensation
Cortical
Subcortical
Mixed
Aging Gracefully: Strategies to slow the process of
aging and risk factors for dementia
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What’s Hot and What’s Not
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As we age, certain aspects of cognition decline, while
others are maintained, or even improved!
One of the most common complaints of older adults
is a decline in memory function… so that will be our
focus today
We will now examine a variety of implicit and explicit
memory tasks to illustrate the neurocognitive profile
(of memory) in healthy older adults
3
What’s Hot and What’s Not
IMPLICIT MEMORY
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What’s Hot and What’s Not
Motor Learning
 Pursuit Rotor Task
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Must keep the tip of a stylus in continuous
contact with a moving target
Motor skill = time spent on target
Motor Learning = increased time-on-target
across repeated trials
Older adults show slower learning
5
What’s Hot and What’s Not
Motor Learning

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Confound of slowed motor speed
Age differences have not been found on
tasks where the task is subject paced
(e.g., learning a sequence of motor
responses)
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What’s Hot and What’s Not
Motor Learning Take Home Message

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Older adults are not as adept as younger
adults at performing motor tasks
BUT
They are equally skilled in learning,
retaining, and transferring motor skills IF
they are allowed to pace themselves during
learning
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What’s Hot and What’s Not
Priming

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Word stem completion  older adults
show priming similar to young
BUT, when asked to recall the word list,
older adults were impaired (just like the amnesic
patients…think back to the memory lecture!)
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What’s Hot and What’s Not
Priming
 Presented with inverted words (450 ms)
 Asked to say words out-loud
 Repeated words on some trials (prime)
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Older adults showed priming like young
Older adults were less skilled at learning the task
Task was slowed to 900 ms
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Age related deficits were abolished
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What’s Hot and What’s Not
Take Home Message on Priming

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Older adults show priming (perceptual,
conceptual and associative)
Are less skilled at learning tasks
BUT
This effect can be abolished if
presentation time is slowed
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What’s Hot and What’s Not
EXPLICIT MEMORY
11
What’s Hot and What’s Not
Semantic Memory

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Older adults show minimal declines in
vocabulary, knowledge of historical facts,
and knowledge of concepts
Older adults can retrieve already learned
semantic information, and can learn new
semantic information
12
What’s Hot and What’s Not
Semantic Memory

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There is an exception to preserved semantic
memory with age
Older adults show difficulty retrieving familiar
words
Tip of the Tongue States  inability to recall a
sought-after word, combined with a strong feeling
that the word is, in fact, known

Suggests selective failure in accessing phonological info
(cues fix the problem)
13
What’s Hot and What’s Not
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Take Home Message for Semantic
Memory
Older adults show preserved semantic
memory
BUT
Have difficulty with word finding, and
are more susceptible to the ‘Tip of the
Tongue’ state
14
What’s Hot and What’s Not
Personal Episodic Memory
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Asked participants to generate memories in
response to cue words
Distribution of memories from most recent
(10-20 yrs) did not differ in relation to age
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Recent memories were most available
Retention decreased with increasing time since
the event occurred
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What’s Hot and What’s Not
Personal Episodic Memory
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Reminiscence Bump  a disproportionate
number of memories from early adulthood
WHY???
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Peak in cognitive performance?
Greater number of significant life events?
Bump overshadowed (in middle-age) by recent
events in middle adulthood?
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What’s Hot and What’s Not
Take Home Message for Personal Episodic
Memory

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Older adults show a profile similar to young
adults
BUT
Older adults show a ‘reminiscence bump’
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What’s Hot and What’s Not
Episodic Memory (text and words)
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Marked declines in recall for text and words
in participants 55+ (16yr longitudinal study)
No deficits in recognition
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What’s Hot and What’s Not
Episodic Memory (text and words)
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It is well established that older adults show
deficits in recall, but NOT recognition
WHY???
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More attentional demand for recall (drain
resources)?
More environmental support in recognition?
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What’s Hot and What’s Not
Take Home Message for Episodic
Memory (text and words)
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Recall for words declines fastest
Recall for text and words is markedly
lower in those +55
BUT
Recognition is spared
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What’s Hot and What’s Not
Visuospatial Memory
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Viewed 20 common objects in one of 4
rooms
Later asked to place the object in the room
it was observed (3, 15, and 30 min delays)
Older adults were less accurate on the
30min delay condition (not on others)
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What’s Hot and What’s Not
Visuospatial Memory
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Subjects followed the experimenter along a
novel route
Older adults were impaired at retracing the
route and ordering landmarks
Unimpaired at recognizing landmarks
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What’s Hot and What’s Not
Visuospatial Memory
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Age-related deficits CAN be reduced, or
even eliminated, but HOW??
Visually distinctive context greatly reduces
visuospatial memory deficits
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What’s Hot and What’s Not
Visuospatial Memory
Take Home Message

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Older adults show visuospatial memory
decline
BUT
Visually distinctive contexts reduce or
eliminate this effect
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What’s Hot and What’s Not
Working Memory
 Reading Span Paradigm
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Read a list of two, three or four sentences
and then recall the last 2 words of the
sentences
Age related declines in span
Can reduce deficit by giving breaks
between trials
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What’s Hot and What’s Not
Working Memory
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Younger adults perform like older adults
when to be remember stimuli is presented
in a noisy environment
Do older adults have a greater vulnerability
to interference from irrelevant or
distracting info?
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What’s Hot and What’s Not
Take Home Message For WM
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Older adults show a decline in working
memory (storage and manipulation)
This may be due to increased
susceptibility to environmental
distractors
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What’s Hot and What’s Not
Prospective Memory (form the intention to carry out an act in the future)
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100 participants, 10 age cohorts (35-80)
Task  to remind experimenter that a form must be
signed at the end of testing
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61% of subjects aged 35-45yrs remembered
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25% of subjects aged 70-80yrs remembered
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What’s Hot and What’s Not
Prospective Memory
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Older adults perform more poorly than young on
laboratory prospective memory tests
Older adults OUTPERFORM younger adults (20’s) on
prospective memory tasks in the real world!!
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Superiority reflects more structured daily lives in older
adults??
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What’s Hot and What’s Not
Take Home Message for Prospective
Memory
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Older adults show declines in prospective memory in
the laboratory
BUT
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Outperform young adults in real-world memory tasks
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They are just more variable…have more momentary lapses
of intention
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What’s Hot and What’s Not
Source Memory (capacity to remember the origin
of our knowledge)
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Participants listen to a series of words read
aloud by either male or female voices
Older adults have more difficulty recalling
the sex of the voice (even when memory
performance for the words is controlled)
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Perceptual deficits??
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What’s Hot and What’s Not
Source Memory
 Source memory deficits are evident even
when sources are not primarily perceptual in
origin
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Older adults do have intact perceptual functions,
but require more effort?
Can reduce or eliminate source memory
deficits
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Highly perceptually distinct stimuli
Consider facts not emotions
Personal rather than general relevance
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What’s Hot and What’s Not
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Take Home Message for
Source Memory
Source memory deficits in older adults are
reliable
BUT
Numerous manipulations can attenuate or
eliminate deficits
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Suggests source memory in not a separate and
impaired system
These results may reflect different ways in which
older adults use strategies
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What’s Hot and What’s Not
False Memory
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Older adults are more susceptible to
misleading post-event suggestion
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For young adults, multiple study-list
exposures results in increased true memory
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For older adults, multiple study-list exposures
results in increased true and false memory
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What’s Hot and What’s Not
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Take Home Message for
False Memory
Older adults are more susceptible to
false memories
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A deficit in source memory? Can’t
remember where info came from?
A deficit of reality monitoring?
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What’s Hot and What’s Not
Meta-Memory (memory beliefs)
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Older adults report deteriorating faculties
regardless of whether they show an increase
in self-reported memory decline
Suggests memory complaints are based on
stereotype rather than evaluation of the self
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What’s Hot and What’s Not
Meta-Memory
 Programs aimed to increase memory selfefficacy improve memory performance
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De-emphasizing the ‘memory’ component and
emphasizing ‘knowledge’ component of
memory tasks eliminates age differences on
some memory tasks
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What’s Hot and What’s Not
Take Home Message for
Meta-Memory
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It’s a matter of mind over matter!!
Memory performance can be improved
by increasing self-efficacy beliefs and
placing emphasis on ‘knowledge’
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What’s Hot and What’s Not:
Summary Page
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INTACT
Motor learning
Priming
Semantic memory (not
word finding)
Episodic Memory for
well-learned life events
Passive short-term
storage of information
Recognition memory
Prospective memory in
the real-world
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DECLINES
WM– especially with
interference
Encoding new
information in deep
elaborative way (less
strategic)
Retrieval (particularly
when effortful)
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Uncued recall,
prospective memory,
recovery of specific
details, source memory
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What’s Hot and What’s Not
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We see that different memory systems are affected
differently by age (more evidence for multiple
memory systems?!)
Why are some functions impaired, while others are
intact?
It seems that functions that are contingent on frontal
integrity are most impaired

We will now briefly touch upon more general deficits
experienced by older adults
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The Frontal Lobes
As we age, the frontal lobes:

1.
2.
3.
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Are the last to mature (into our 20’s)
Show the greatest reduction in blood flow (later in
life)
Show the greatest amount of tissue loss (later in
life)
Not surprisingly, older adults often show
deficits on neuropsychological tests that are
considered ‘frontal’
(think back to the executive functions lecture…and about
strategies used to remember things)
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The Frontal Lobes
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Older adults show deficits on task like:
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Self-ordered pointing
Wisconsin Card Sorting Test
Verbal Fluency (FAS)
Stroop Task
Working Memory Tasks
Prospective-memory tasks
Source Memory Tasks
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Parietal Lobes
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The parietal lobes are also susceptible
to the effects of aging, though not to
the extent of the frontal lobes
Right hemisphere constructional and
visuomotor tasks
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Temporal Lobes
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As discussed, older adults show deficits on
declarative memory tasks
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Problems on recall (not so much recognition)
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Problems strategically searching through
memory to retrieve memory (frontal too??)
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Related to loss of hippocampal tissue
(extreme cases of Alzheimer’s Disease)
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Theoretical Frameworks:
Memory Decline in Older Adults
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Decline in Processing Speed
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Decreased processing speed underlies
many of the cognitive deficits noted in
older adults
Memory is not impaired, per se, but is due
to slow mental processing or difficulties
with timing of complex mental functions
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Evidence: experimenter paced motor learning
tasks
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Theoretical Frameworks:
Memory Decline in Older Adults
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Depletion of Attentional Resources
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Reduced attentional resources to carry out
mental functions
Observe differences between performance
of simple (stable) and complex (decline)
tasks
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Evidence: tasks requiring more effort (e.g., free
recall, prospective and source memory)
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Theoretical Frameworks:
Memory Decline in Older Adults
Age-Related Inhibitory Deficits
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Older adults are less efficient at inhibiting
partially activated representations
Inhibitory functions play three important roles in
memory:
1.
2.
3.
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Provides control over access to WM (i.e., restrict access
to task relevant info)
Supports deletion of irrelevant information from WM
Provides restraint of pre-potent responding
Evidence: age-differences in WM tasks
interference???
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Theoretical Frameworks:
Memory Decline in Older Adults
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Decreased Cognitive Control
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Older adults suffer from an impairment in
executive control of cognitive processing
Relies on distinction between automatic
(unconscious) and controlled (effortful) processes
Automatic processes are immune to the effects of
aging while controlled processes demonstrate
decline (combo of reduced resources & inhibitory deficit theories)
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Evidence: can account for WM, episodic, source
prospective, false….maybe too much? Need to
understand more about executive functions
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Laterality in Older Adults
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Think back to the hemispheric specialization
lecture……
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Recall that certain functions are lateralized within the
brain…can you think of some examples?
HAROLD
Hemispheric Asymmetry Reduction in Old Adults
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Episodic memory retrieval, episodic encoding/semantic
retrieval, working memory, perception, and inhibitory control
Evidence using both functional neuroimaging and
electrophysiological methodologies
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Dedifferentiation Hypothesis
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Reduced hemispheric asymmetry in old adults
may reflect and age-related difficulty in
recruiting specialized neural mechanisms
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 asymmetries are just another example of the
deleterious effects of aging on the brain
Evidence: correlations among different
cognitive measures increase with age
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Compensation Hypothesis
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Increased bilaterality in old adults could help
counteract age-related neurocognitive deficits
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 asymmetries are an example of the brain reorganizing to
compensate for the effects of aging
Evidence: as a result of contralateral recruitment, cognitive
functions that are strongly lateralized in the healthy brain
may become more bilateral following brain damage
Evidence: Following L hem stroke, better language recovery
is observed in aphasic patients with bilateral activation
(fMRI)
51
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Evidence for the
compensation
hypothesis
High performing older
adults show bilateral
activation
Low performing older
adults show lateralized
activation
52
DEMENTIAS
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Dementias
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Recent medical and technological advances have increased the
average life expectancy of Canadians
Consequence  aging population that is plagued with
neurodegenerative disease = poor quality of life and lost
productivity

Estimated 280,000 Canadians have Alzheimer’s Disease
(5.5 billion $/year)
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By 2031, an estimated 3-4 million Canadians will have
Alzheimer’s Disease
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Economic impact is large  long disease duration, high cost of
healthcare, lack of effective treatments
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Dementias
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Dementia  an acquired and persistent syndrome of
intellectual impairment
DSM-IV defines the two essential diagnostic features
of dementia:
1.
2.
•
Memory and other cognitive deficits
Impairment in social and occupational functioning
Typically progresses in stages: mild, moderate and
severe (eventually leads to death)
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Dementias:
Three Broad Categories
Cortical
1.
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Alzheimer’s disease, Pick’s disease and
Creutzfeldt-Jacob disease
Subcortical
2.
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Parkinson’s disease, Huntington’s chorea
Mixed
3.
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Vascular dementia a.k.a. multi-infarct dementia
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Alzheimer’s Disease: History

First recognized 100 years ago by Alois Alzheimer
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1906  presented data on patient ‘Auguste D’, a 51-year-old
woman with “delerium and frenzied jealousy of her husband”
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Alzheimer claimed that her dementia was caused by gross
neuroanatomical lesions identified in her brain post-mortem

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Observed “milliary bodies” and nerve cells that were choked by
“dense bundles of fibrils”
“Clinicopathological era”  scientists began to investigate the
correlates of clinical symptoms and pathology (something that
was not accepted until that time)
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Alzheimer’s Disease: History

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1960’s  autopsies of patients with ‘senility’ confirmed what
Alzheimer had claimed
In most cases there were clearly visible deposits of beta-amyloid
plaques (“milliary bodies”) and intracellular deposits of
neurofibrillary tangles (“dense bundles of fibrils”)
Today, AD can only be definitively diagnosed post-mortem
Characterized by the accumulation of neuritic plaques
composed of amyloid-beta peptide fibrils, and neurofibrillary
tangles of hyperphosphorylated tau within the limbic and
neocortical areas of the brain
58
Alzheimer’s Disease: Pathology


Healthy individuals
produce beta-amyloids
(protein fragments) that
are quickly broken
down and removed by
the body
In AD, these proteins
accumulate between
neurons and form hard,
insoluble plaques
59
Alzheimer’s Disease: Pathology


Neurofibrillary tangles
composed of twisted fibres
inside the neuron consisting of
the protein tau, which form
microtubles, which are
responsible for the transport of
nutrients in and out of the cell
In AD the tau protein is
abnormal and causes
neurofibrillary tangles which in
turn cause the microtubule
structure to collapse
60
Cortical Dementia:
Alzheimer’s Disease

AD is also characterized by a severe loss of
cholinergic innervations in the cerebral cortex,
an overall decrease in brain volume, and
enlargement of ventricles
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Alzheimer’s Disease: DSM-IV

The DSM-IV lists four separate diagnostic criteria for
Alzheimer’s disease dependent on:
1.
2.
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the time of onset (earl versus late)
the presence of delirium, delusions, or depressed mood
In simple terms  late onset uncomplicated AD =
gradual development of multiple cognitive and
memory deficits including aphasia, apraxia, agnosia,
and executive dysfunction
Disturbance of everyday function, must progress
steadily, and must not be attributable to some other
Axis I disorder, caused by systemic conditions (e.g.,
vitamin deficiency), or substance abuse
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Alzheimer’s Disease:
Progression
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Early stages  memory deficits caused by degeneration of
neurons in the hippocampus
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During this initial stage of the disease, there are no motor, sensory
and co-ordination deficits
As progresses  extends to the cerebral cortex affecting the
frontal lobes, deficits in judgement, decision making, inhibition,
personality, mood, language and communication are observed
Final stages  the ability to recognize faces and communicate
is completely abolished, followed by loss of bladder and bowel
control, and finally death
The average time from diagnosis to death is approximately 10
years
63
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Cortical Dementia:
Alzheimer’s Disease
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Memory
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Global anterograde amnesia
Retrograde amnesia (temporally graded)
Deficits in short-term memory
Procedural memory is not spared
How are Alzheimer’s disease patients
similar and different from medialtemporal-lobe amnesia patients?
65
Cortical Dementia:
Alzheimer’s Disease

Language

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Aphasia
Semantics are more affected (FAS)
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Name as many animals as possible 
Name as many words that begin with letter ‘F’
Emotional functioning

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Neurotic
Anxious
Introverted
Passive
Less agreeable
66
Cortical Dementia:
Alzheimer’s Disease

Therapeutic Interventions

Drugs targeting the cholinergic system


Drugs that block acetylcholine (e.g., scopolamine) cause memory
impairments in healthy individuals
Increase the amount acetylcholine facilitates memory

Drugs that block acetylcholinestarase (the enzyme that
breaks down acetycholine) have been somewhat
successful (e.g., tacrine)
Many side effects

These drugs just slow the progression of the disease

67
Cortical Dementias:
Frontotemporal Dementia
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Pick’s disease (type of frontotemporal dementia)
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15-20% of dementias
Changes in social-emotional functioning
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Language
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Lack of inhibition
Impulsivity
Shoplifting
Lack of concern for social norms
Perseveration
Lack of insight
Obsessed with food
Poor naming
Difficulties in reading and writing
No deficits in spatial processing and memory (at least early on)
68
Cortical Dementias:
Frontotemporal Dementia

Physiological characteristics
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Atrophy of frontal and temporal
lobes
Neurons are pale and swollen
‘ballooned’
Pick’s bodies in the cytoplasm
(rather than neurofibrillary
tangles)
Presents primarily in the realm of
social-emotional functioning (think
of the OFC patients)
69
Cortical Dementias:
Creutzfeldt-Jacob Disease

1 in a million = RARE!

Caused by prions (proteinaceus infectious particles)

Prions are normal proteins found in the brain, but they
can undergo a change of shape and become insoluble

Thus, cannot be broken down, they accumulate and
lead to cell death

Incubation period is quite long
70
Cortical Dementias:
Creutzfeldt-Jacob Disease

Prions are highly transmittable (e.g., corneal
transplants, contact with infected brain tissue)

Eating cattle with spongiform encephalopathy (mad
cow disease)

Behavioural decline is MUCH quicker than
Alzheimer’s or frontotemporal dementia

Individuals live about a year after dementia diagnosis
71
Subcortical Dementias:
Huntington’s Disease

GABAergic neurons in the striatum (caudate, putamen, globus
pallidus) are destroyed leading to excess movement

Jerky, rapid, uncontrolled movement

Almost always leads to dementia

Deficits in:
 Executive function
 Switching mental sets, inhibition (WCST), planning
 Spatial processing
 Memory
 Much better at recognition than recall (unlike AD)
 No temporal gradient equal memory impairment across
time (unlike AD)
72
Subcortical Dementias:
Parkinson’s Disease
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Loss of DA neurons in substantia nigra
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Dementia occurs in about 30% of individuals

Deficits
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Impoverishment of feeling, motive (emotion,
desire or physiological need) and attention
Slowing of motor and thought bradyphrenia
Executive functions (WCST, Tower of London)
Spatial memory
73
Mixed Varieties Dementias:
Vascular Dementias

AKA: Multi-Infarct Dementia

Caused by many small strokes (obstruction of blood flow) that create
both cortical and subcortical lesions

2nd most common type of dementia

When restricted to the subcortical white matter, dementia is referred to
as Binswanger’s disease

In contrast to other dementias, the onset is quite rapid (following
stroke) abrupt onset vs insidious onset in AD

There can be fluctuations in symptoms

Display predominantly problems with executive function ,verbal fluency
and attention (FRONTAL LOBES)
74
Risk Factors and Strategies for
Aging Gracefully
Protective Factors
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Non-steroidal antiinflammatory drugs ↓
Higher education ↓
Mentally challenging work
and activity ↓
Estrogen replacement
therapy (women) ↓↑???
Risk Factors

APOE-4 allele =
↓ cholinergic activity
↑ density of senile plaques

Smoking ↑

Cardiovascular disease ↑

Diabetes ↑

Head injury ↑
75
What you should know…



Describe the deficits and spared functions observed
in healthy older adults, and provide evidence to
support your statement (implicit, explicit)
Describe the theories of cognitive decline and provide
one piece of evidence for each theory
Describe the dedifferentiation and compensation
hypothesis of delateralization and supporting
evidence
76
What you should know…

Describe the cortical, subcortial and mixed
dementias


Know cognitive profile of each, be able to compare
and contrast dementias
Be aware of the risk factors associated with
dementia, and strategies for
improving/maintaining function later in life
77