Essay 5: Outline and Evaluate Disorders of Memory

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  • Essay 5: Outline and Evaluate Disorders of Memory
    • AMNESIA
      • There are 2 types of Amnesia: Retrograde (forgetting OLD info) and Anterograde (forgetting NEW info)
      • 1) Damage to Hippocampus
        • Damaging the hippocampus can cause amnesia
        • Infection
          • Case Study= Clive Wearing
            • STM intact but unable to lay down new LTM
            • LTM for events prior to illness
              • Procedural memory was intact
                • But declarative and episodic memory was affected
            • Viral encephalitis damaged his hippocampus and adjoining areas of temperal lobes
        • Surgical Brain injury
          • Case study=HM (Scoville and Milner):
            • HM also improved in mirror drawing skills with successive trails even though he couldnt recall doing it before
            • HM's Hippocampus surgically removed in order to reduce epileptic fits.
              • STM intact and LTM for events prior to surgery intact, However,  HM is unable to lay down new LTM
              • HM improved in the Golen test ( recognising incomplete line drawings) with successive trails even though he couldnt remember having done the test before
        • Evaluation of Brain Danage Theory
          • However studies dont specify which area leads to memory loss
          • Case studies of BD patients infer that BD to specific areas causes specific memory loss.
          • It appears that areas within or close to the Hippocampus are involved in semantic and episodic memory loss.
      • 2) Explicit V.S Implicit memory ( Schachler)
        • Can used HM and Clive Wearing as case studies
        • Explicit memory requires conscious recollection, whereas Implicit doesnt.
        • Contrlled experiments
          • Graf et al (1984)
            • Lab experiment. Word list was presented to amnesiac patients with an immediate recall test
              • Amnesiac's recall was much worse than controls for explicit memory tests but equal on the implicit test
            • 3 out of 4 tests were conventional explicit memory, where the 4th involved implicit memory
          • Stickgold (2000)
            • People with normal memory can learn tetris in a few hours and describe it. whereas peo+
            • People with normal memory can learn tetris in a few hours and describe it. whereas people with Amnesia can improve, showing implicit memory but have no explicit memory of having done so
        • Evaluation: All of the previous sugests that amnesisa may be caused by impairment in explicit/ declarative memory
          • This explanation is descriptive rather than explanatory
          • Ryan et al (2000)
            • Through relational memory binding suggested that amnesiac lack the function which makes a link between implicit and explicit memory which is also known as consolidation
      • 3) Impairment of consolidation of information
        • Ryan et al (2000)
          • Through relational memory binding suggested that amnesiac lack the function which makes a link between implicit and explicit memory which is also known as consolidation
        • Issac and Mayers (1999)
          • They suggested that Anterograde Amnesia might be due to problems with consolidation or retrieval of memories.
          • They found that Amnesia performed as well as controls on cued recall and recognition
          • This suggests that the main explanation for anterograde amnesia is impairment of consolidation of information rather than retrieval
          • Retrograde Amnesia may also be caused by impaired consolidation as recvall for events occuring closest to onset of amnesia is worst
          • The greater the time between old memories being formed and the onset of Amnesia the better the recall
          • The Temporal Gradient suggests that the greater the consolidation the better the recall
        • This process is associated with damage to the hippocampus suggesting that this brain area plays a key role in forming LTM
          • What causes problems with consolidation?: problems with consolidation may be due to damage to the hippocampus
            • Clive Wearing had a virus which affected his brain, damaging the hippocampus amongst other parts
            • E.g HM, His amnesia was caused by surgery that removed his hippocampus, amygdala and parts of the temporal lobes
        • Reed and Squire (1998)
          • It also suggests that other structures are important
          • This supports the role of the hippocampus in consolidating memory
          • MRI scans of patients with retrograde amnesia showed hippocampus damaage
          • Those with the worst sympotms aslo had damage to the temporal lobe
        • Animal studies.
          • Case studies of humans with naturally occurring brain damage are problematic in that the extent of brain damage varies and so do sympotms
          • Remondes and Schuman (2004)
            • It also suggests that the hippocapmus is associated with consolidation
            • This suggests the rats could make new memories but couldn't consolidate them.
            • Rats with damage to the hippocampus could learn a maze but forgot it quickly.
          • Surgical lesianing of animals' brains offers researchers control in the area of brain being studied.
        • Evaluation
          • Case studies
          • Face Vadlity
          • Use of animals
    • ALZHEIMERS
      • Tau Protein
        • Tangles
          • These were formed from a build up of Tau Protein.
          • Tangles arise when the structure of the neurons' cell body degenerates.
          • This normally provides support for the structure with in a neuron.
          • Tangles are seen in other diseases but have a distinct form in AD.
      • B amyloid
        • Individuals with Alzheimer's don't break down Amyloid precursor protein (APP) properly
        • B-amyloid Plaques
          • Plaques cause damage to cerebral cortex, hippocampus and basal forebrain
          • Plaques interfere with NMDA
            • Cleary et al (2005)
              • Injecting rats with B-amyloid disrupts memory
                • Unable to learn maze
                • Shows cause and effect although can't generalise rats to humans
            • Snyder (2005)
              • B-Amyloid protein 42 interferes with NMDA, a Neurotransmitter which produces changes in neurons when we learn
          • Berntson et al (2002)
            • Alzheimer's effects memory is because of damage to the basal forebrain which is involved with alertness and attention
              • MSM says that in order to commit things to memory you first have to pay attention to them
        • Selkoe (2000)
          • Plaques start to form before symptoms of Alzheimer's. Progressive damage causes cerebral cortex to shrink
            • So suggests that plaques cause Alzheimer's.
              • Previous studies have suggested that the hippocampus is involved in LTM e.g. Clive Wearing
            • Previous studies have suggested that the hippocampus is involved in LTM e.g. Clive Wearing
        • Evaluation of B-Amyloid Plaque Theory
          • The explanation that the basal forebrain is damaged usefully explains why people with AD are less alert and find attending to stimuli more difficult
            • The basal forebrain is involved in increasing arousal in cerebral cortex
              • MSM attention= memories
          • Dogs develop more B-amyloid with age and also develop associated cognitive dysfunction. However, they don't lose neurons or develop plaques and tangles
          • Primates have the same B-amyloid as human but don't develop nerve damage or cognitive symptoms in old age
          • Studies have mainly been carried out on animals even though no single species had all the same physiological and psychological symptoms as human AD patients
          • Generlisability?
          • However the link between the build up of plaque and AD is weak and hard to explain
            • Murphy and LeVine (2010)
              • The presence of  B-amloid protein 42 early in the disease starts a chain of events that leads to the illness
                • This has yet to be tested
          • The explanation that the hippocampus ids damaged usefully explains memory loos in AD
            • Use studies showing a link between memory and hippocampus.
              • E.G Clive Wearing
      • Alzheimer's is the gradual deterioration in cognitive abilities including mempory
        • Compared to Amnesia which is a sudden loss due to brain damage
      • Genetics
        • Lott (1982)
          • Most individuals with Downs syndrome (DS) Who reach middle age develop early onset Alzheimer's
          • As DS is caused by having an extra copy of chromosome 21, this led researchers to look for and find genes associated with AD on Chromosome 21
        • Levy-Lahad et al (1995)
          • Early onset AD's gene found on Chromosome 1
          • All found different Genes so less reliable
            • Schellenberg et al (1992)
              • Early onset AD's gene found on chromosome 14
              • Ertekin et al (2000)
                • Gene for later onset AD's found on chromosome 10
            • Ertekin et al (2000)
              • Gene for later onset AD's found on chromosome 10
            • AD is a complex disorder, so it's only right that its got a complex cause
        • Schellenberg et al (1992)
          • Early onset AD's gene found on chromosome 14

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