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ALZHEIMER’S DISEASE
INTRODUCTION
 Alzheimer's disease is a
progressive disorder that causes brain cells to
degenerate and die. It is the most common
cause of dementia — a continuous decline in
thinking, behavioral and social skills that
disrupts a person's ability to function
independently.
 AD is the most common neurodegenerative
disorder and it is clinically defined by a slowly
progressing loss of cognitive functions, primarily
memory impairment.
Prevalenceand
ImpactofAD
 AD is the most common cause of
dementia in people 65 years and older
 Affects 10% of people over the age of 65
and 50% of people over the age of 85
 Annual treatment costs = $100 billion
 AD is the fourth leading cause of death
 The overwhelming majority of patients
live at home and are cared for by family
and friends
TheProgressof
Alzheimer
disease
Alzheimer’s Disease
Progresses Through
Distinct Stages
PathologyOfAD
 There are 3 consistent neuropathological
hallmarks:
 –Amyloid-rich senile plaques
 –Neurofibrillary tangles
 –Neuronal degeneration
 These changes eventually lead to clinical
symptoms, but they begin years before the
onset of symptoms
BETA-amyloid
Plaques
 Plaques form when protein pieces
called beta-amyloid clump together. Beta-
amyloid comes from a larger protein found
in the fatty membrane surrounding nerve
cells. Beta-amyloid is chemically "sticky"
and gradually builds up into plaques.
PLAQUE
FORMATION
Neurofibrillary
Tangles
 Neurofibrillary tangles (NFTs) are
aggregates of hyperphosphorylated tau
protein that are most commonly known as
a primary marker of Alzheimer's disease.
Their presence is also found in numerous
other diseases known as tauopathies.
Cholinergic
Hypothesis
Acetylcholine (ACh) is an
important neurotransmitter in
areas of the brain involved in
memory formation
Loss of Ach activity correlates
with the severity of AD
TREATMENT
Primary goals: to enhance quality of
life & maximize functional
performance by improving
cognition, mood, and behavior
–Nonpharmacologic
–Pharmacologic
NONPHARMACOLOGI
C
Cognitive enhancement
Individual and group therapy
Regular appointments
Communication with family,
caregivers
Environmental modification
Attention to safety
PHARMACOLO
GIC
Cholinesterase inhibitors: donepezil,
rivastigmine, galantamine
Other cognitive enhancers: estrogen,
NSAIDs, ginkgo biloba, vitamin E
Antidepressants
Antipsychotics
Acetylcholines
terase
Inhibitors
 Drugs used to treat Alzheimer’s disease act by
inhibiting acetylcholinesterase activity
 These drugs block the esterase-mediated
metabolism of acetylcholine to choline and
acetate. This results in:
 –Increased acetylcholine in the synaptic cleft
 –Increased availability of acetylcholine for
postsynaptic and presynaptic nicotinic (and
muscarinic) acetylcholine receptors
THANKYOU

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Alzheimer's disease

  • 2. INTRODUCTION  Alzheimer's disease is a progressive disorder that causes brain cells to degenerate and die. It is the most common cause of dementia — a continuous decline in thinking, behavioral and social skills that disrupts a person's ability to function independently.  AD is the most common neurodegenerative disorder and it is clinically defined by a slowly progressing loss of cognitive functions, primarily memory impairment.
  • 3. Prevalenceand ImpactofAD  AD is the most common cause of dementia in people 65 years and older  Affects 10% of people over the age of 65 and 50% of people over the age of 85  Annual treatment costs = $100 billion  AD is the fourth leading cause of death  The overwhelming majority of patients live at home and are cared for by family and friends
  • 6. PathologyOfAD  There are 3 consistent neuropathological hallmarks:  –Amyloid-rich senile plaques  –Neurofibrillary tangles  –Neuronal degeneration  These changes eventually lead to clinical symptoms, but they begin years before the onset of symptoms
  • 7. BETA-amyloid Plaques  Plaques form when protein pieces called beta-amyloid clump together. Beta- amyloid comes from a larger protein found in the fatty membrane surrounding nerve cells. Beta-amyloid is chemically "sticky" and gradually builds up into plaques.
  • 9. Neurofibrillary Tangles  Neurofibrillary tangles (NFTs) are aggregates of hyperphosphorylated tau protein that are most commonly known as a primary marker of Alzheimer's disease. Their presence is also found in numerous other diseases known as tauopathies.
  • 10. Cholinergic Hypothesis Acetylcholine (ACh) is an important neurotransmitter in areas of the brain involved in memory formation Loss of Ach activity correlates with the severity of AD
  • 11. TREATMENT Primary goals: to enhance quality of life & maximize functional performance by improving cognition, mood, and behavior –Nonpharmacologic –Pharmacologic
  • 12. NONPHARMACOLOGI C Cognitive enhancement Individual and group therapy Regular appointments Communication with family, caregivers Environmental modification Attention to safety
  • 13. PHARMACOLO GIC Cholinesterase inhibitors: donepezil, rivastigmine, galantamine Other cognitive enhancers: estrogen, NSAIDs, ginkgo biloba, vitamin E Antidepressants Antipsychotics
  • 14. Acetylcholines terase Inhibitors  Drugs used to treat Alzheimer’s disease act by inhibiting acetylcholinesterase activity  These drugs block the esterase-mediated metabolism of acetylcholine to choline and acetate. This results in:  –Increased acetylcholine in the synaptic cleft  –Increased availability of acetylcholine for postsynaptic and presynaptic nicotinic (and muscarinic) acetylcholine receptors

Editor's Notes

  1. The Mini-Mental State Examination (MMSE) or Folstein test is a 30-point questionnaire that is used extensively in clinical and research settings to measure cognitive impairment