Alzheimer's Disease - Amherst



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

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