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How do we think we form memories We are not completely sure how we form memories. Neuropsychologist Karl Lashley once said "We may know that limited regions.

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Presentation on theme: "How do we think we form memories We are not completely sure how we form memories. Neuropsychologist Karl Lashley once said "We may know that limited regions."— Presentation transcript:

1 How do we think we form memories We are not completely sure how we form memories. Neuropsychologist Karl Lashley once said "We may know that limited regions may be essential for learning and retention but these regions do not as such house memory" - Fundamentals of Human Neuropsychology 3rd ed Kolb, B. and Whishaw, I.Q. Do we form memories because we need to remember something or do we remember something because we have memories to retain experiences. The answer to this question was once a complete mystery to us but scientists have now been able to decipher some of the mechanisms that aid the complex function of memory.

2 Memories are formed……… When? Memory consolidation takes time, event initiates a molecular cascade. Where? Hippocampus and associated cortical structures. Memories are then distributed probably over the cerebral cortex but we are still unsure. How? Synaptic re-organization is crucial. Modulation of structural, adhesion neurotransmission proteins. Susan Keogh 08"

3 MEMORY CATEGORIES  Short-Term: Few seconds up to approx. 1 day. 7 digit phone number, Number plate etc. Serotonin (5-HT), main transmitter involved Ceases if not consolidated.

4 Synaptic Communication. This diagram shows transmission at a synaptic cleft, the synaptic vessicles are stimulated by a electrical impulse and the neurotransmitter is released and it interacts with the receptors. Susan Keogh 08"

5 The Case of H.M Dr William Scoville performed a prefrontal lobotomy on H. M in1953. Temporal lobe from both hemispheres of HM’s brain removed. HM was left with severe amnesia. He can no longer form new long term memories. Dr William Scoville 1906-1984

6 Removed: Amygdale Perirhinal cortex, Entorhinal cortex 2/3 of Hippocampus

7 Hippocampus and synaptic plasticity Thanks to H.M we know that the hippocampus is vital for memory formation. However the fact that H.M retains his long term memory indicates this is not where memories are stored. The early stages of memory consolidation are associated with structural changes within the hippocampus. In the first 24 hours after learning something there are 1000 to 1500 proteins changing in our brain and the number of nerve connections doubles. Susan Keogh 08"

8  Long-Term Memory Consolidation by ‘Rehearsal’. Weeks to Years. Chemical and structural changes (plasticity) Declarative- Conscious retrieval of learned fact. Can be stated. “I had a maths exam last week” Procedural- Unconscious. Difficult to verbalise, E.g. Bicycle riding.

9 Long Term Potentiation (LTP)  Lasting enhancement of synaptic transmission.  Occurs all areas known to be involved in memory  Hippocampus CA3→CA1  Glutamate main transmitter involved  NMDA and AMPA channels  Calcium and Sodium dependant  Ca/Calmodulin and protein kinase C stimulate retrograde second messenger to presynaptic neuron  Plasticity

10 CREB a molecular switch for long term memory?? Several intracellular signalling pathways are induced by neural activity but CREB phosphorylation seems to be important to convert memories into long term storage. Behavioral experiments carried out in Drosophilia established that over expression of CREB activator enhances long term memory. Link to website showing experiment: bin/;page=Helicon_ CREB bin/;page=Helicon_ CREB Susan Keogh 08"

11 When the CREB pathway is stimulated repeatedly, it regulates the expression of genes involved in a synaptic growth process, which ultimately changes the connections among neurons in the circuit. These changes in synaptic connections, distributed throughout the circuit, represent the physical basis of long-term memory. Susan Keogh 08"

12 Memory storage Stimulus Sensory organs Short term memory Long term memory Repetition, retieval and forgetting Amnesia The loss of ability to recall usually easily retainable information and the inability to form new memories. Anterograde Amnesia: cannot form memories after a specific point Retrograde Amnesia: cannot recall memories before a specific point Transient Global Amnesia: sudden, random memory loss Amnesia suffers sometimes regain memory with therapy over time however once brain cells are damaged they cannot be reformed so recollection is uncommon. Sources: fundamentals of Human Neuropschology,

13 Korsakoffs syndrome Korsakoff's syndrome is a memory loss associated with long term alcholism and hence a thaimine deficiency. Symptoms: anterograde and retrograde amnesia, made up stories, poor conversational skills, low attention spans, double-vision, staggering and drooped eyelids. Memories are rarely completely regained but thiamine rich diets can help.

14 Huntington’s Disease and Memory Loss Huntington’s Disease (H.D.) or Huntington’s Chorea is defined as,“ A distinct familial presenile dementia with a novel missense mutation in the Tau Gene”. In simpler terms H.D. is a neuro degenerative disease which is passed on hereditarily and results in certain cognitive and physical symptoms which adversely affect a person’s lifestyle and mental capability. A person suffering from H.D. will experience dysfunction over time of working memory and procedural memory. Working memory can be described as short term, while on the other hand procedural memory can be described as how we remember how to swim or play a musical instrument. Huntington’s Disease slowly wastes away nerve cells in the brain. Although it is not entirely clear exactly how it does this, it is a fact that the Huntingtin protein is present throughout the body and is necessary for growth and development. Many scientists believe that the altered or flawed version of this protein has an adverse reaction with nerve cells in the brain which leads to the onset of the adverse symptoms associated with H.D. Another part of how neurologists believe the disease mechanism works is that neurons in the brain try to unsuccessfully degrade abnormal Huntingtin, which results in widespread atrophy or wasting away of the caudate and frontal lobe, along with other areas of the brain. Since an accurate genetic test was established in 1983 for the DNA marker related to H.D. research into treatment and understanding of the disease has greatly increased. Treatments regarding drugs, general care and nutrition among patients have alleviated some of the stress and hardship that sufferers undergo.

15 Alzheimer’s Disease as a cause of Memory Loss Dementia describes various conditions which damage brain cells and leads to loss of brain function over time. Dementia causes a progressive decline in mental ability. It describes loss of memory, rationality, social skills and the ability to emotionally respond. Alois Alzheimer first set out the parameters of symptoms which he observed in a patient in 1901. He defined this woman’s mental decline as a physical disease rather than a natural progressive loss of brain function. A.D. currently affects 26 million people worldwide and as of yet no effective treatment has been established. This illness can adversely affect how memories are formed. Over time the disease attacks the cortex and hippocampus more than other areas of the brain. When A.D. presents itself in a healthy brain, protein strands begin to twist and tangle. As they do so they begin to damage local neurons. When enough neurons are damaged, brain function becomes compromised. This picture shows us how A.D. damages and degenerates the brain over an extended period where normal ventricles have been transformed into cavernous voids. In the past treatment for sufferers of A.D. have been directed more so at families of patients for whom it is very difficult to manage with this person’s degeneration. Although drugs that have been in use have been moderately successful in delaying the onset of this neuro-degeneration, the future of treatment is relatively bright. More sophisticated treatments are under construction which will hopefully keep memory function intact and rapidly decrease rate of degeneration of neurons and the tangling of protein strands. When all is taken into account early diagnosis of Alzheimer’s Disease along with treatment can significantly reduce the stress on patients and family members alike.

16 See how well your brain forms memories! Short term memory tests -Letters tests - Picture games - Facial visual tasks - Match arcade Long Term Memory links: 2.html 2.html

17 References Link to interview with HM: =7584970&m=7584971 =7584970&m=7584971 Corkin, S. (2002). What’s new with the amnesic patient H. M.? Nat. Rev. Neurosci. 3: 153-160. Scoville, W. B. & Milner, B. (1957). Loss of recent memory after bilateral hippocampal lesions. J. Neurol. Neurosurg. Psychiat. 20: 11-21. “Cognitive Neuroscience” The Biology of the Mind, Michel S. Gazzangia, Richard B. Ivry, George R. Mangun, Second Edition 2002 Norton – picture of Dr William Scoville picture of H.M’s brain Keith Murphy’s lecture notes for BMOL 20030 bin/;page=Helicon_CREBwww.mdconsult.com bin/; St. Davnet’s Mental Hospital Monaghan American Huntington’s Disease Foundation












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