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  1. Memory Year 12 Psychology Unit 3 Area of Study 2 (Chapter 6, Page 286)

  2. Neural Basis of Memory • Memories are not stored in one specific brain location; they are stored throughout the brain and linked together by neural tracts (interconnected neurons). • Also known as neural pathways or ‘memory circuits’. • Not all areas are equally involved in memory: • Different areas/structures active as we encode/store/retrieve. • Certain brain areas are more or less involved in different memory processes: • E.g. temporal lobes active for declarative explicit memories, but less important for procedural implicit memories.

  3. Neurons in Memory Formation • Structure & functioning of neurons in the brain change when forming memories of newly learned experiences. • Connections between neurons are strengthened, making communication easier the next time. • Each time a memory is recalled, neurons in the relevant circuit are activated: • Repeated activation strengthens the connection; • “Neurons that fire together, wire together”.

  4. Neurons in Memory Formation

  5. Hippocampus & Temporal Lobe • Hippocampus: in lower region of each temporal lobe, just above ear, 4cm into brain, shaped like a seahorse, about 3.5cm long. • Involved in formation of new long-term memories, but are not memory storage sites. • Important role in formation and/or encoding of new declarative explicit memories (semantic & episodic). • Not involved in formation or retrieval of implicit procedural memories. • Not involved in short-term memory storage. • Hippocampus = ‘memory formation area’, integrating information to create whole memories.

  6. The Case of H.M.Video • Henry Molaison suffered severe epilepsy; in 1953 (he was 27 years old) he had surgery to treat it. • Doctors removed both of his medial temporal lobes: • Inner surface area near middle (medial) of temporal lobe, consisting of hippocampus, amygdala and other cortical tissue. • H.M. was left with anterograde amnesia: • Remembered events before his surgery, but could not form new long-term episodic or semantic memories. • Short-term memory remained normal – as long as he actively rehearsed something (maintenance rehearsal) he could retain it, but as soon as he became distracted the memory information was lost.

  7. AMYGDALA • It is an almond shaped group of nuclei • Directionally, the amygdala is located deep within the temporal lobes, medial to the hypothalamus and adjacent to the hippocampus. • Shown to have a vital role in the processing of emotions which can help determine which memories should be stored and where in the brain. • Not a storage site

  8. Consolidation Theory • Physical/structural changes to neurons in the brain occur when something new is learned and immediately after learning. • New information transferred from STM to LTM needs time to consolidate (‘strengthen’ or ‘set’). • If memory formation is disrupted during the consolidation phase, information may not be properly embedded in LTM and may therefore be lost. • Consolidation is vulnerable for at least 30mins, but could continue for as long as several weeks or years.

  9. Evidence for Consolidation Theory • The case of H.M. (hippocampus and medial temporal lobe play important roles in consolidation). • Memory loss as a result of brain trauma (e.g. being bumped on the head, encephalitis, ECT): • Unable to remember events immediately prior to trauma or anything that happened for 30mins after trauma. • Rats given ECT immediately after, 20sec after, 30mins after or 60mins after running a maze: • Only rats given ECT after 60mins could accurately remember the task – consolidation period for rats is approximately 60mins.

  10. Reconsolidation… Activity: 6.29 • After a memory is activated and retrieved from LTM, it needs to be reconsolidated in order to be returned to LTM storage. • Explains why our memories can change over time. • Gazzaniga & Heatherton (2006): • Rats accurately retrieved information from LTM; • Rats were injected with a drug that interfered with the reconsolidation process; • They were later unable to accurately recall that same information.

  11. Memory Decline Over the Lifespan • Research studies indicate that there may be some naturally occurring decline in some aspects of memory among older people. • BUT memory decline is not an inevitable consequence of ageing. • If a decline in memory is experience through ageing, effects are more likely to be on working/STM & declarative memory (sematic & episodic), rather than procedural memory.

  12. Memory Decline Over the Lifespan:Effects of Ageing on STM • Impact depends on the nature of the task: • Simple tasks = STM is not affected by age. • Complex tasks (divided attention; simultaneous storage & manipulation of) = age-related factors may impact on effective STM functioning. • 60+ years of age: decrease in the activation of areas of the frontal lobes of the brain believed to be involved in STM. • Nervous system is less efficient at receiving and transmitting info; therefore rate/speed info (esp. numbers & words) is processed in STM is slower.

  13. Memory Decline Over the Lifespan:Effects of Ageing on LTM • Poorer episodic memory, but minimal decline in procedural or semantic memory. • Episodic can begin decline as early as 30 or late as 50. • Take longer to learn new info & skills – incl. info that would be stored as semantic & procedural memories. • It seems that older people do not encode new info with a much detail or as precisely as young people. • Speed and fluency of retrieval of info from semantic memory may decline with age.

  14. Memory Decline Over the LifespanEffects of Ageing on LTM Ch. 6 Test • Explanations for memory changes; • Lack of motivation: for example, lack of motivation to perform well during psychological experiments. • Lack of confidence: having low confidence can worsen the problem of declining memory. • Lack of access to info from LTM is influenced by measure of retention that is used: recall is more affected than recognition… retrieval cues help. • Cognitive Slowing: • CNS functioning slows, unable to mentally process info with the same speed and efficiency. • Possibly caused by the reduction in size of the frontal lobes.

  15. Amnesia Resulting from Brain Trauma & Neurodegenerative Diseases. • Brain Trauma: ‘umbrella’ term for any damage that impairs/interferes with normal functioning. • Inflicted Brain Injury: intentional violence against brain. • Acquired Brain Injury: accident, disease, stroke, surgery, etc. • Neurodegenerative Disease: characterised by progressive decline in structure, activity & function of brain tissue. • Degeneration is typically age-related. • Amnesia: partial/complete, permanent/temporary memory loss commonly as a result of brain trauma. • May ‘improve’, leaving only residual amnesia. • Many different kinds (see page 343).

  16. Amnesia:Anterograde Amnesia • Loss of memory for info or events after person sustains brain damage. • Info prior to damage still remains, but cannot remember what has happened since. • Explained by the ‘Information-Processing Model of Memory’: • Info enters sensory memory, is attended to & transferred to STM. • Can be manipulated in STM & rehearsed indefinitely, but the brain structures involved in transferring it from STM to LTM are damaged, therefore no new permanent memories can be formed. • Korsakoff’s Syndrome: • Neurodegenerative disease: damage to hippocampus & thalamus. • Common in alcoholics due to thiamine (vitamin B) deficiency. • Typically appear normal but cannot form new memories (and may also have extensive loss of past memories) • Hard to determine actual memories, as sufferers often attempt to ‘fill the gaps’ (known as confabulating).

  17. Anterograde Amnesia ExamplesVIDEOS: 1 & 2

  18. Amnesia:Retrograde Amnesia Activity: 6.31 • Loss of memory for info or events experienced before person sustains brain damage. • Memory loss may extend back a few moments, days, weeks or sometimes years. • Usually temporary and often caused by a blow to the head. • Experienced by patients of electroconvulsive therapy (ECT). • Memory of the period immediately before the accident is often never recovered. • Explained by the ‘Information-Processing Model of Memory’ • Interruption to the consolidation of the memory trace. • Memory trace was forming as info processed from STM to LTM. • At time of brain trauma, consolidation process was interrupted - memory of info & events just prior to the injury won’t have had time to consolidate, so likely to be lost from memory altogether.

  19. Dementia • Umbrella term: variety of symptoms of a large group of illnesses or neurodegenerative diseases that cause progressive decline in a person’s mental functioning. • Most common symptom is serious loss of mental capacity, including: • Memory loss; • Decline in intellectual ability; • Poor judgement; • Poor social skills; • Abnormal emotional reactions

  20. Dementia • Often described as progressing in stages (first sign is typically memory loss). • Memory loss is persistent & progressive. • Usually develops over a number of years, gradually getting worse: • Not normal part of ageing process; • Most people who age do not develop dementia; • More than 60 known diseases/illnesses (most are neurodegenerative) can cause dementia symptoms; • Neurodegenerative cause = usually irreversible.

  21. Alzheimer’s Disease • Neurodegenerative disease characterised by gradual widespread degeneration of brain neurons: • Memory loss; • Decline in cognitive & social skills; • Personality changes. • Currently 4th largest cause of death in Australia. • Post-mortems show that brain has appearance of being ‘rusted’: ‘blobs’ of ‘plaque’ deposits, tangles of brain fibres, damaged neuronal connections.

  22. Alzheimer’s Disease • Neurons shrink and eventually disappear (‘die’) at a greater rate than normal: • Disrupts communication within the brain; • As it progressively affects different brain areas, those functions or abilities are lost. • Approx. 100 000 Australians suffer Alzheimer’s: • One in twenty-five people over the age of 60; • One in eight people over the age of 65; • One in four people over the age of 80; • Affects some people in their mid-50s; • Estimated that number of sufferers will increase by 40% in the next decade.

  23. Alzheimer’s Disease:Diagnosis • Currently no single or simple diagnostic test for Alzheimer’s disease: • Accurate diagnosis can only be made from autopsy; • Physical signs are not readily detectable in living patients; • Tests of memory, intellect, personal skills and general knowledge are used to determine the rate of mental deterioration (in absence of physical tests). • There is no one symptom that is reliable; • Specific symptoms experienced will differ per person; • Early symptoms are memory loss (starting with typical incidents of understandable forgetfulness), confusion, unusual irritability, impaired decision-making.

  24. Alzheimer’s Disease:Memory Loss • Events: • All or part of an event. • Words or names: • Progressively forget words & names of people & things. • Written & verbal directions: • Progressively lose ability to follow directions. • Stories on TV, in movies or books: • Progressively lose ability to follow stories. • Stored knowledge: • Lose known information such as history or politics. • Everyday skills: • Progressively lose ability to perform tasks such as dressing and cooking.

  25. Alzheimer’s Disease:Additional Symptoms • Severe personality changes: • Polite & quiet rude & loud. • Caring & outgoing apathetic & withdrawn • Lapses in judgement: • Combined with memory loss, makes daily functioning very difficult (e.g. eating, taking medication). • Inability to recognise people: • Family members, regular carers, or even themselves.

  26. Alzheimer’s Disease:What Happens in the BrainVideo • Abnormally high levels of the protein amyloid: • Neurotoxic– poisons brain cells, causing cell death; • Insoluble– cannot be metabolised by the brain; • Causes development of plaques (deposits of protein & cell materials outside/around other neurons) and tangles (twisted fibres built up outside the neuron). • Hippocampus & related areas of the midbrain appear to be most affected: • Up to ¾ of neurons in these areas may be lost & the others are often damaged. • Greatly reduced levels of the neurotransmitter acetylcholine: • VIDEO • Associated with intellectual functioning, especially memory & learning.

  27. Alzheimer’s Disease:The Verdict Activity: 6.33 • Currently there is no known cure. • Medications that increase supply of acetylcholine can slow the rate of degeneration if started during early or middle stages of the disease. • Pet and MRI scans are frequently used to identify extent of brain damage, making it possible to identify which parts (and therefore functions) have deteriorated. See figure on page 350.

  28. Memory Websites! • •