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L08.AD - Alzheimer's Disease Edward Koo M.D Department of...

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Alzheimer's Disease Edward Koo, M.D. Department of Neurosciences Shiley-Marcos Alzheimer's Disease Research Center University of California, San Diego BIPN 150 Diseases of the Nervous Systen January 29, 2009
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Incidence of Alzheimer's disease 55 65 75 85 95 0 2 4 6 8 10 New Cases/100/year AD Incidence Rates E. Boston Rochester Hisayama Lundby Framingham Rochester In 2000, U.S. Population was 280 million 12.5% over age of 65 (35 million) 15% over age 65 have dementia (5.3 million) Two-thirds due to Alzheimer's disease (3.5 million)
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Progressive, irreversible brain disorder Gradually destroys memory and ability to learn, reason, communicate, make judgments, and carry out daily activities Fatal (death usually occurs within 8 ² 10 years of diagnosis) 4th leading cause of death for Americans over 65 37 million affected worldwide What is Alzheimer · s Disease?
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Symptomatology and progression of AD AD progression Mild ± MMSE >20 Forgetfulness Problems with shopping, etc. Depression Mod ± MMSE 10-20 Severe ± MMSE<10 Ƃ Impairment of recent memory Ƃ Require help with ADLs Ƃ Delusions Ƃ Limited language Ƃ Loss of basic ADLs Ƃ Agitation, incontinence
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What are neurodegenerative diseases? Progressive loss of neurons with associated astrogliosis and secondary white matter changes Selective loss of neurons (by region, transmitter systems, etc.) No inciting events that predispose to these changes Rare genetic mutations produce virtually identical diseases Occasional pathological hallmarks, etc. Lewy bodies in Parkinson's disease Examples: Alzheimer's disease, Huntington disease and other polyglutamine disorders, Creutzfeldt-Jakob disease (aka ´ prion diseases µ , ´ mad cow µ ), Parkinson's (loss of dopaminergic neurons), multi-system atrophies
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Idiopathic Parkinson's disease
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Ƃ What causes it in most cases Ƃ How to definitively diagnose it in live patients Ƃ How to prevent it Ƃ How to treat it Ƃ 4 medicines approved for amelioration of symptoms Ƃ 0 medicines currently available to treat underlying disease There · s a lot we don · t know about AD
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Alzheimer's Pathology Senile (amyloid) plaques Neurofibrillary tangles Neuronal loss Synapse loss Inflammatory responses
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Alzheimer · s Disease Pathology Amyloid Plaques and Neurofibrillary Tangles Neuronal Degeneration and Loss of Synapses Impaired Neuronal Activity Normal Alzheimer s Disease Normal Alzheimer s Disease Brain Atrophy
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Why are synapses lost and why do neurons die in AD? AD control control AD
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Alzheimer's pathology
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A b is released after two cleavages and deposited in senile plaques in brain
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1970s: Description of cholinergic deficiency and cholinergic hypothesis 1984: Purification of ǀ -amyloid from plaques (Glenner, UCSD) 1985: Demonstration of tau protein in tangles 1987: Cloning of the APP gene Early 1990s: Description of APP mutations that cause AD
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