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Progress Report on Alzheimer’s Disease Taking the Next Steps NIA NIH Alzheimer’s Disease (AD) • • • • • • Age-related Irreversible brain disorder Occurs gradually Results: memory loss behavior/personality changes decline in thinking abilities • • • • Course of disease varies from person to person Rate of decline varies Ave. after Dx: 8-10 years Advances from mild forgetfulness to severe loss of mental fx • Symptoms appear after 60 • EARLY LATE – loss of recent memory faulty judgement & personality changes – easily confused forget simple tasks • FINALLY: – become completely dependent on others for everyday care – become debilitated, likely to develop other illnesses/infections – Usually die of pneumonia • “Although the risk of developing AD increases wih age, AD and dementia symptoms are not a part of normal aging”. (p.2) IMPACT OF AD • Most common cause of dementia among those 65& older • Up to 4 million currently have AD • Prevalence doubles every 5 years beyond age 65 • Numbers are bound to increase as the population ages • A Question: Are there differences in AD risk, incidence & prevalence among various racial/ethnic groups? • Why? #s of over-65 non-Caucasians is growing rapidly--increase from 16 to 34% by 2050 • African Americans & Hispanic Americans may have higher overall risk of AD Impact of AD • Heavy economic burden on society--annual cost of care: – mild AD:$18,408 – moderate AD: $30,96 – severe AD: $36,132 – Tremendous caregiver burden • Impact of delaying AD onset: an enormous public health impact • Fed AD research areas: – causes/risk factors – diagnosis – treatment/caregiving General AD Progress • Destruction of cells in hippocampus--failure of short term memory and easy tasks become more difficult • Attack on cells in cerebral cortex--loss of language skills & judgement-making abilities • As more & more of the brain becomes involved (atrophies): – – – – – Personality changes Emotional outbursts Wandering Agitation Finally--bedridden, incontinent, helpless & unresponsive to outside world Main AD Features: Plaques & Tangles • Amyloid Plaques – Insoluble deposits of beta-amyloid – portions of neurons – non-nerve cells such as microglia – Are they a cause, or an effect of AD? Neurofibrillary tangles • Primary component: tau proteins, which normally stabilize a cell’s internal support structure by binding and stabilizing microtubules Types of AD • Familial AD (FAD)--early onset--only 5-10% of cases • Sporadic AD--late onset Brain changes with normal aging • Some neurons in some regions die--most important to learning don’t • Some neurons shrink & function less well • Tangles & plaques develop in some regions • Inflammation increases • Oxidative stress increases • Free radicals--product of normal metabolism • --may be helpful to cells in fighting infection • --highly reactive • Production of too many is oxidative stress Exploration of rel. of AD with other “diseases of aging” • Possible link between brain infarcts & AD • Blood cholesterol and rate of plaque deposition. • Parallels between AD & other progressive neurodegenerative disorders--all involve deposits of abnormal proteins in the brain Can AD be treated? • FDA has approved 3 meds – – – – 1993: Cognex 1996: Aricept 2000: Exelon Slows symptom advance, but will not stop or reverse AD – Act by inhibiting acetylcholinesterase (enzyme that breaks down a key neurontransmitter) AD Research areas/goals • Understanding etiology of AD • Improving early Dx • Developing drug Tx’s • Improving support for caregivers