Download Dementia - Amherst College

Memory Impairments: Dementia
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1) Discuss some basic issues regarding dementia
(including Alzheimer's Disease) including
incidence, symptoms, diagnoses and causes.
2) Examine the particular memory deficits found in
 Episodic memory
 Autobiographical memory
 Semantic Memory
 Implicit Memory
 Procedural Memory
3) Discuss attempts to ameliorate the memory
differences observed in dementia.
Dementia – The basics
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Incidence:
 5.3 million people
o Higher incidence in women than men
 13% of people over 65
 1 new case per minute
 5th leading cause of death of people over 65
Time course:
 Early Stage
o Minor memory problems
EX: Word-finding problems (Lindy)
o Mild disorientation / confusion
 Middle Stage
o Slowly develop more pronounced, very
broad memory difficulties
o Disorientation / confusion
o Day-to-day variability
o Depression
EX: Driving Sydney
 End stage
Dementia: Diagnoses / Causes
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Alzheimer's Disease
Via autopsy
 neuritic plaques
 Clumps of diseased cells
 neurofibrillary tangles
 look like tumbleweed
 Located throughout brain
 concentrated in MTL
 Reduced brain weight
 contributes to a lack of acetylcholine
Reduced metabolic activity
Causes:
Unknown
 genes, smoking, education, head injuries
Difficulties: gender
Distinguishing dementia from amnesia:
1) IQ
2) Orientation
3) Confabulation
4) Semantic memory
Measurement - MMSE
Other forms of dementia
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Vascular dementia:
 Reduced blood flow
 TIA / small strokes
 Memory often not as impaired as in AD
Dementia with Lewy bodies
 Similar to AD
 Daily fluctuation
 Hallucinations, ridigity, tremors
 Parkinson’s Diesease
Frontotemporal dementia
 Language problems
 Personality changes
 Pick’s disease
Hydrocephalus
 Fluid build in the brain
 Difficulty walking, urination
Deficits in AD – Episodic Memory
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Declarative memory
Deficits across the board
EX: Creative fashion
SP effects remain intact
Delay is the key:
Q: What brain structure does this implicate?
Recognition deficits are less than recall deficits
Q: What does that imply about the cause?
Encoding? Storage? Retrieval?
Autobiographical memory
 Same distribution as healthy adults, but many
fewer memories
 Temporal gradient
EX: Sydney's recollection of my family
No consensus in the literature.
Encoding? Storage? Retrieval?
Deficits in AD – Semantic Memory
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Huge deficits
 Used to stage the disease
EX: fluency measures
 Better with pictures than definitions
 No LOP effect
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Encoding? Storage? Retrieval?
Consistency – if a subject fails to identify a picture of
a common object, s/he will be unlikely to respond
correctly when given the definition.
EX: Famous face / name tests
Problems with consistency:
 Retrieval failures can produce 'consistent'
behavior
EX: What if an organized search terminates
early?
Identifying the Cause of Semantic Memory
Deficits in AD: Rohrer, et al. (1999)
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Theoretical Question: Do semantic memory deficits
in AD result from the loss of stored information,
or from impaired retrieval?
Empirical Question: Will AD patients' produce
relatively fast RTs on a verbal fluency task?
Previous work suggesting storage problems:
 Subcategory cues do not aid category fluency
 Fewer specific examples
 Category fluency worse than letter fluency
o Different patterns from HD
Previous work suggesting retrieval problems:
 Normal semantic priming
 Sentence completion RT correlated with
difficulty
 Some show no differences in deficits on
category vs. letter fluency
Key piece of data: RT is directly related to the size of
the category: more members====>slower RTs.
EX: College / grad school admission
Rohrer, et al. (1999)
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Results:
Both patient groups produced fewer items
AD
faster than age-matched controls
HD
slower than age-matched controls
Interpretation:
 AD patients respond faster because there are
fewer items stored in memory
 Therefore, dementia patients suffer a loss of
stored information.
Points to ponder:
Do these data unambiguously prove that Rohrer
et al.'s interpretation is correct?
 Age differences b/t patient populations
and corresponding control groups
 late papers
Rohrer et al.’s (1999) data
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Deficits in AD – Procedural Memory
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AD patients can still do many everyday tasks:
EX: folding laundry (highly idiosyncratic)
Also learn standard laboratory tasks at roughly the
same rate (when difficulty is controlled)
 pursuit tasks
 implicit sequence learning
Motor-encoding enhances explicit memory
Pick up the cup
Subsequent memory is better for performed
actions relative to imagined actions or read
statements.
Deficits in AD – Memory Interventions
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Things that seem to help
 Imagery
EX: Link item to prominent facial feature
 Self-reference / generation
EX: own cues much better than E cues
 Personal items
EX: own object vs. unfamiliar exemplar
 Errorless learning
EX: Trained on famous faces using
vanishing cues
no guess instructions
 Music
EX: Schulkind and Cespedes (2002)
Fischer, Sananbenesi, Wang, Dobbin, & Tsai (2007)
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Neuron death is a problem: can we reverse neuron
death and in so doing, restore previously learned
information?
Multiple experiments:
1. Establish that drugs cause neurodegeneration
a. How did they do that?
2. Establish that neurodegeneration inteferes with
memory
a. How did they do that?
3. What was the cause of the memory loss?
a. Storage (loss of neurons)
b. Retrieval (loss of synaptic connections)
4. How did they examine this question
a. Introduced EE
5. Why was EE effective?
a. Restored synapses in ACC
b. How?
i. Modifies genes to promote plasticity
ii. But can’t rule out additional neurons
Killam, Cautin, & Santucci (2005)
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Experimental question: Are college athletes with a
history of concussions impaired relative athletes with
no history and/or non-athletes?
“Tissue deforming collisions with the internal wall
of the skull”
Multiple injuries associated with:
 Significant mental impairment
 Depression
 Stress management
Precautions
 Self-diagnosis
 Objective diagnosis
 Objective diagnosis under stress
 However, participation may be enough
Method:
 DIII athletes in contact (??) sports
 Matched for: gender, ethnicity, year, GPA,
 Concussion index scores (# x severity)
 RBANS, post-concussion checklist, Stroop
Killam, et al. (2005): Results and Discussion
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Results:
 Group Differences (Fisher’s LSD):
o Athletes – concussed or not – were worse on
immediate/delayed memory
o No differences on other subtests or Stroop
o No differences in concussive symptoms
 Negative correlations b/t concussive symptoms:
o attention and delayed memory
o Recovery in non-recent concussed group
o Stroop task: processing speed is affected
Discussion
 Immediate memory is particularly vulnerable,
but appears to recover
 Non-concussed athletes < controls
o GPAs were equivalent (??)
o Sub-clinical damage (??)
 Self-assessment is inadequate
 More rest to protect from neuropsychological
damage