chap13-Amnes

chap13-Amnes - CHAPTER 13 AMNESIA and Hippocampal Function...

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CHAPTER 13 – AMNESIA and Hippocampal Function The two types of amnesia : - retrograde: loss of memory for events that occurred prior to the brain damage/event that caused memory impairment. - bump on the head and you forget who you are and who you know, but you remember all events that occurred after the incident. - impairment severe for recent memory; old memories maintained. - anterograde: memory loss for events that occur after the brain damage/event. - you can remember the past, but not anything that has happened since the event-- unable to learn new information. - is the defect in encoding (learning) or storage or recall? For both types of amnesia, are all categories of memories equally affected? Many brain areas have been linked to amnesia specifically, and learning and memory in general. - medial temporal lobes (MTL) - hippocampus plus the amygdala plus the limbic cortex: - entorhinal cortex, parahippocampal cortex and perirhinal cortex - diencephalon (thalamus, hypothalamus), - cerebral cortex, striatum, cerebellum, etc. Two themes for this section: 1) How have we learned which brain areas regulate specific features of learning and memory? - animal and human studies 2) What is the function of different brain areas—are there different memory systems that control or underlie different aspects or types of learning and memory???? Consider human studies first: Human Models for Memory – study of people with brain damage. A. Neurodegenerative diseases or illnesses- study of patients with memory defects associated w/ these disorders have also suggested brain regions involved in memory. - Alzheimer’s Disease – most common form of dementia - progressive disease: depression and general decline in cognitive ability early on, then irritability, anxiety, speech problems and ultimately loss of control of basic bodily functions
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- cholinergic neurons in basal forebrain (and other regions) most susceptible to degeneration. - brain becomes overwhelmed by neurofibrillary tangles (tangles of protein in cytoplasm) and amyloid plaques (clumps of scar tissue). - found most prevalently in medial temporal lobe structures (as well as in cortex) - familial form (early onset; 5-10% of cases) versus late onset form - defect in the APP (amyloid precursor protein) gene? l - Korsakoff’s syndrome - alcoholics - lack of vitamins-- in this case thiamine (vitamin B1) , which is required for metabolic breakdown of fats, carbohydrates and proteins. - alcoholics stop eating, or eat poorly, in part because they are not hungry due to high calories in alcohol; also, alcohol inhibits absorption). - severe brain damage can result from intravenous infusion of glucose (given to malnourished patients), which builds up and damages neurons because it can’t be metabolized. - damage (for some reason) appears most severe in the
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chap13-Amnes - CHAPTER 13 AMNESIA and Hippocampal Function...

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