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 memoryfaulty judgement & personality changes –easily confusedforget 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