Download PowerPoint Presentation - Progress Report on Alzheimer`s Disease

Progress Report on Alzheimer’s
Disease
Taking the Next Steps
NIA NIH
Alzheimer’s Disease (AD)
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Age-related
Irreversible brain disorder
Occurs gradually
Results: memory loss
behavior/personality changes
decline in thinking abilities
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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
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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):
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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
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--may be helpful to cells in fighting
infection
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--highly reactive
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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
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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