Alzheimer's Disease



Memory Impairments: Alzheimer's Disease

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1) Discuss some basic issues regarding Alzheimer's Disease (AD) 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 AD.

Alzheimer's Disease – The basics

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Incidence:

15% of people over 65; 45% of people over 85

And the country is getting older

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

Alzheimer's Disease – Diagnoses / Causes

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Diagonsis:

Via autopsy

• neuritic plaques

←

• neurofibrillary tangles

←

• Located throughout brain

←

• Reduced brain weight

←

Reduced metabolic activity

Causes:

Unknown

• genes, smoking, education, head injuries

Difficulties:

Distinguishing dementia from amnesia:

1) IQ

2) Orientation

3) Confabulation

4) Semantic memory

Measurement - MMSE

Deficits in AD – Episodic Memory

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Declarative memory

Deficits across the board

EX:

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

• Temporal gradient

EX: Sydney's recollection of my family

No consensus in the literature.

Encoding? Storage? Retrieval?

Fromholt & Larsen (1991)

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Deficits in AD – Semantic Memory

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Huge deficits

• Used to stage the disease

EX:

• 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:

Problems with consistency:

• Retrieval failures can produce 'consistent' behavior

EX:

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 than age-matched controls

HD than age-matched controls

Interpretation:

• AD patients

• Therefore, dementia patients suffer

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:

• Self-reference / generation

EX:

• Personal items

EX:

• Errorless learning

EX:

• Music

EX: Schulkind and Cespedes (2002)

Fischer, Sananbenesi, Wang, Dobbin, & Tsai (2007)

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Question: 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 interferes 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 – were

o No differences on

o No differences in

• Correlations – concussive symptoms were:

o Predicted attention and delayed memory

o Recovery in non-recent concussed group

o Processing speed on Stroop

Discussion

• Immediate memory is

• Non-concussed athletes < controls

o GPAs were equivalent (??)

o Sub-clinical damage (??)

• Self-assessment

• More rest

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