Explanations for disorders of memory

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  • Created by: gracepxx
  • Created on: 09-04-16 13:14

P1 - Intro

Many people develop illness which leads to impaired memory

Amnesiacs - unable to recognise faces, name them or recall that they knew them

Alzhiemers disease - cognitive problems such as hallucinations & memory loss

Attempts are made to explain impacts on memory

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P2 - Describe amnesia

One effect of amnesia - loss of explicit memory 
Schacter (1987) - Forgetting in amnesiacs explained by impaired explicit memory - better at implicit memory tasks (not requiring consious recollection) than explicit (require)
Example - HM and the Golin test - recall improved with repetiton but couldn't recall ever having done the test before
Explains why amnesiacs can do procedural memory tasks (physical skills) but not ones testing declarative memory (fact related) - HMs skill to draw using mirror but didn't know that he could do it

Amnesiacs also have inability to consolidate new memories 
Anterograde amnesia - cannot form new LTMs - Issac & Mayes (1999) suggested may be due to problems with consolidation or retrival of memories 
Tested amnesiacs alongside control group - amnesiacs performed as well as controls - issues with consolidation rather than retrieval 
Reterograde amnesia - loss of memory for past events - recall of memories may improve over time - change indicates LTMs need to be consolidates otherwise lost
Amnesiac symptoms cause disruption to consolidate due to damage of hippocampus - plays key role in forming LTMs. 

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P3 - Evaluate amnesia

Stickgold et al (2000) used tetril to show amnesiacs could learn a new task like "normal" people (implicit memory) but not recall it (explicit)

However, Schacter et al (1995) - re-presenting learned words in pairs in the same voices helped "normal" Ps not not amnesiacs 

Shows despite usually finding explicit tasks harder - not always true - cannot always learn implicitly 

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P4- Describe alzhiemers

Also attempted to identify explanations for alzhiemers

One cause - a faulty protein (b-amyloid) is produced in brain and builds up between neurons forming plaques
Plaques prevent the neurons from communicating and damages the cerebal cortex, causing it to shrink
Berntson et al (2002) - plaque damage affects memory possibly because it causes AD 
Snyder et al (2005) - maybe because b-amyloid interfers with a neurotransmitter involved in learning

Tangles could also be explanation for AD
Tau protein builds up on brain of people with AD - normally supports structure of neurons but in AD it forms tangles inside cell bodies of neurons when they die

Several genes associated with AD have been found
People with down's syndrome often have early onset AD - DS caused by extra copt of chromosone 21 so researchers tend to look for genes related to AD here
Genes found that affect production of b-amyloid explaining why some more likely to develop AD

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P5 - Evaluate alzhiemers

Link between plaques and cognitive problems is weak, making it hard to see how plaques could cause AD
However, Murphy & LeVine (2010) suggested that b-amyloid triggers chain of events causing damage that continues irrespective of b-amyloid levels
Would mean plaques cause AD no matter how much b-amyloid is present but explanation is yet to be tested
Role of b-amyloid studied using animals - different from human patients - loss of cognitive functions not comparable and no formation of plaqurd or tangles in animals - can't generalise

St George-Hyslop (2000) - effects of genes on AD must be small as about half of patients have no relatives who are sufferers


Cleary et al (2005) - found injecting rats with b-amyloid disrupted memory

Hock et al (2003) - deterioration in memory prevented when the immunte system is triggered and destrys patients b-amyloid - suggests protiein is a big part of AD

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