1. INTRODUCTION
Alzheimer's disease is a degenerative
brain disorder of unknown etiology which
is the most common form of dementia, that
usually starts in late middle age or in old
age, results in progressive memory loss,
impaired thinking, disorientation, and
changes in personality and mood. There is
degeneration of brain neurons especially in
the cerebral cortex and presence of
neurofibrillary tangles and plaques
containing beta-amyloid cells
2. Origin of Alzheimer's Disease
The disease was first described
by Dr. Alois Alzheimer, a German
physician, in 1906. Alzheimer had a
patient named Auguste D, in her
fifties who suffered from what
seemed to be a mental illness. But
when she died in 1906, an autopsy
revealed dense deposits, now called
neuritic plaques, outside and around
the nerve cells in her brain. Inside
the cells were twisted strands of
fiber, or neurofibrillary tangles.
Since Dr. Alois Alzheimer's was the
first person who discovered the
disease, AD was named after him.
Auguste D
3. Meaning
Alzheimer’s disease is a chronic, irreversible
disease that affects the cells of the brain and causes
impairment of intellectual functioning.
Alzheimer's disease is a brain disorder which
gradually destroys the ability to reason, remember,
imagine, and learn.
4. Comparison of a normal aged brain
(left) and an Alzheimer's patient's
brain (right). Differential
characteristics are pointed out.
5. INCIDENCE
About 3 percent of men and women
ages 65 to 74 have AD, and nearly half
of those age 85 and older may have the
disease.
About 3,60,000 new cases of
Alzheimer’s are diagnosed each year.
6. CAUSES
The cause of Alzheimer’s disease is
not known.
However, several factors are thought
to be implicated in this disease.
8. 2.ENVIRONMENTAL FACTORS
• Cigarette smoking.
• Certain Infections.
• Metals, industrial or other toxins.
• Use of cholesterol lowering drugs
(statin).
9. 3 . GENETIC AND IMMUNOLOGICAL
FACTORS
Oxidized LDL receptor 1 and
Angiotensin 1-converting enzyme, are tied
to the way the brain cells bind to
Apolipoprotein4 (APOE4) and reduce
buildup of harmful proteins, known as
plaques, in the brain, respectively.
10. RISK FACTORS
a) Down's syndrome.
b) Family History.
c) Chronic high BP.
d) Head injuries.
e) Gender.
f) Smoking and Drinking
11. PATHOPHYSIOLOGY
• Alzheimer's disease attacks nerves and brain
cells as well as neurotransmitters.
• The destruction of these parts causes clumps of
protein to form around the brain's cells. These
clumps are known as 'plaques' and 'bundles'.
The presence of the 'plaques' and 'bundles' start
to destroy more connections between the brain
cells, which makes the condition worse.
12. DUE TO THE ETIOLOGICAL FACTORS
CHANGES OCCUR IN THE PROTIENS OF THE NERVE CELLS
OF THE CEREBRAL CORTEX
ACCUMULATION OF NEUROFIBRILLARY TANGLES AND PLAQUES
GRANULO VASCULAR DEGENERATION
LOSS OF CHOLINERGIC NERVE CELLS
LOSS OF MEMORY, FUNCTION AND COGNITION
13. Microscopy image of a neurofibrillary tangle,
conformed by hyperphosphorylated tau
protein
14.
15. • Enzymes act on the APP (amyloid precursor protein) and
cut it into fragments. The beta-amyloid fragment is
crucial in the formation of senile plaques in AD
16. In Alzheimer's disease, changes in tau protein lead to the
disintegration of microtubules in brain cells.
17. SIGNS
Ten warning signs of Alzheimer's disease
1)
2)
3)
4)
5)
6)
7)
8)
9)
10)
Memory loss
Difficulty to performing familiar tasks
Problems with language
Disorientation to time and place
Poor or decreased judgment
Problems with abstract thinking
Misplacing things
Changes in mood or behavior
Changes in personality
Loss of initiative
18. SYMPTOMS
• Confusion
• disturbances in short-term memory
• problems with attention and spatial orientation
• personality changes
• language difficulties
• unexplained mood swings
20. PET scan of the brain of a person with AD showing
a loss of function in the temporal lobe
21. Pharmacological intervention
• Acetylcholinesterase inhibitors -prevent the
breakdown of acetylcholine, a chemical
messenger important for learning and memory
eg. Donepezil (Aricept)
Rivastigmine (Exelon)
Galantamine (Razadyne
22. N-Methyl d-aspartate Receptor Antagonist
(NMDA)
• Eg:Memantine – blocks the NMDA
receptor and inhibit their overstimulation
by glutamate (neurotransmitter)
•
•
•
•
Antidepressents.
Anxiolytics.
Antipsychotics.
Anticonvulsants
24. Caregiving
Since Alzheimer's has no cure and it
gradually renders people incapable of
tending for their own needs, caregiving
essentially is the treatment and must be
carefully managed over the course of the
disease
25. Prognosis
• The early stages of Alzheimer's disease are difficult to
diagnose. A definitive diagnosis is usually made once
cognitive impairment compromises daily living activities,
although the person may still be living independently. He
will progress from mild cognitive problems, such as
memory loss through increasing stages of cognitive and
non-cognitive disturbances, eliminating any possibility of
independent living.
• Life expectancy of the population with the disease is
reduced. The mean life expectancy following diagnosis is
approximately seven years. Fewer than 3% of patients
live more than fourteen years. Disease features
significantly associated with reduced survival are an
increased severity of cognitive impairment, decreased
functional level, history of falls, and disturbances in the
neurological examination.
26. • Other coincident diseases such as heart problems,
diabetes or history of alcohol abuse are also related with
shortened survival. While the earlier the age at onset the
higher the total survival years, life expectancy is
particularly reduced when compared to the healthy
population among those who are younger. Men have a
less favourable survival prognosis than women.
• The disease is the underlying cause of death in 70% of
all cases.Pneumonia and dehydration are the most
frequent immediate causes of death, while cancer is a
less frequent cause of death than in the general
population.