1. Progress Report on Alzheimer’s Disease
Taking the Next Steps
NIA NIH

2. Alzheimer’s Disease (AD)
Age-related
Irreversible brain disorder
Occurs gradually
Results: memory loss
behavior/personality changes
decline in thinking abilities

3. 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

4. Symptoms appear after 60 EARLY LATE
loss of recent memory faulty judgement & personality changes
easily confused forget simple tasks

5. FINALLY: become completely dependent on others for everyday care
become debilitated, likely to develop other illnesses/infections
Usually die of pneumonia

6. “Although the risk of developing AD increases wih age, AD and dementia symptoms are not a part of normal aging”. (p.2)

7. 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

8. 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

9. 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

10. Impact of delaying AD onset: an enormous public health impact
Fed AD research areas:
causes/risk factors
diagnosis
treatment/caregiving

11. 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

12. As more & more of the brain becomes involved (atrophies):
Personality changes
Emotional outbursts
Wandering
Agitation
Finally--bedridden, incontinent, helpless & unresponsive to outside world

13. 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?

14. Neurofibrillary tangles
Primary component: tau proteins, which normally stabilize a cell’s internal support structure by binding and stabilizing microtubules

15. Types of AD Familial AD (FAD)--early onset--only 5-10% of cases
Sporadic AD--late onset

16. 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

17. Free radicals--product of normal metabolism
--may be helpful to cells in fighting infection
--highly reactive
Production of too many is oxidative stress

18. 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

19. 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)

20. AD Research areas/goals
Understanding etiology of AD
Improving early Dx
Developing drug Tx’s
Improving support for caregivers