Disorders of Memory

Mark Scheme


·         Statistical abnormalities (tip of the tongue, onomastic aphasia)

·         Psychological disorders (repression, PTSD)

·         Pathological disorders (Alzheimers and Amnesia)


·         Evidence relating to specific issues

·         Evaluation of explanations for statistical abnormalities

·         Evaluation of psychological disorders

·         Discussion of what is a disorder of memory and what are true disorders

·         Processes or organic illness

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·         Partial or total loss of memory, temporary or permanent

·         Caused through accidental impact, brain operations and degeneration

·         Fugue state occurs where we forget our identities, very rare

·         Tip of the tongue, onomastic aphasia and déjà vu

·         Studied through animal research and autopsy making it poorly understood 

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Loss of explicit memory

·         Schacter (1987) amnesiacs are better at implicit memory tasks, rather than explicit that require conscious thought

·         HM could perform the Gollin Test (implicit task) this is procedural not declarative

·         Stickgold (2000) tetris task, amnesiacs could learn new tasks (implicit) but could not explain how to do the task (explicit)

·         Schacter et al (1995) word pairs in the same voice helped normal participants, not amnesiacs, showing memory is not always implicit

·         Ryan et al (2000) relational memory binding – amnesiacs lose the function to link implicit and explicit memory 

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·         Anterograde – prevents new LTM forming

·         Retrograde – can’t recall prior LTMs

·         Temporal gradient, older memories are easier to recall, consolidation is disrupted

·         Issac and Myers (1999) could retrieve memories but not consolidate them, meaning amnesiacs were good on recall but not recognition

·         Gabrieli (1998) CA1 hippocampus damage causes anterograde amnesia

·         Reed and Squire (1998) temporal lobe damage causes worsened affects

·         Remondes and Schman (2004) rats with damage to the hippocampus could learn new maxes but forgot them quickly, showing there is a problem with consolidation 

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Alzheimer’s disease - Β amyloid 42

·         Faulty β amyloid 42 protein produced in Alzheimer’s patients

·         This forms plaques between neurones which leads to damage in the cerebral cortex, hippocampus and basal forebrain

·         Berntson et al (2002) basal forebrain damage leads to impaired alertness and attention

·         Snyder et al (2005) β amyloid 42 interferes with NMDA neurotransmitter which produces change to neurones when we learn

·         Link is poor and lacking evidence

·         Murphy and Levine (2012) β amyloid causes a destructive chain of events, regardless of its concentration

·         Amyloid levels in animals does not seem to have an effect on memory 

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·         Tau protein builds up

·         Causes cell body to disintegrate

·         Evidence is very weak and few studies showing such evidence

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·         Down syndrome patients often suffer early onset Alzheimers

·         Levy-Lehad et al (1995) chromosome 1 link found

·         Schellenberg et al (1992) chromosome 14 link

·         Later onset is found on chromosome 10 – Ertekin – Taner et al (2000)

·         All affect β amyloid production

·         St Georges Hislop (2000) ½ all Alzheimers patients have no relatives with the disease

·         Hendrie (2001) other cultures have the same frequency in other cultures but there is no such prevalence in the disease 

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Korsakoff Psychosis

·         Caused by alcohol abuse

·         Degeneration of brain tissue

·         Impacts the structure of the forebrain 

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