Ms. Ritika Soni presented on Alzheimer's disease. Alzheimer's is a progressive brain disorder that causes memory loss and cognitive decline. It was first described by Dr. Alois Alzheimer in 1906 from examining a patient with unusual brain abnormalities. The causes are not fully known but risk factors include age, family history, and head injuries. Diagnosis involves cognitive assessments and brain imaging. Currently, there is no cure, but medications and caregiving can temporarily improve symptoms.

1.  Presenter:
 Ms. Ritika soni

2. INTRODUCTION
 Alzheimer's disease is the commonest
progressive, dementing, neurodegenerative
brain disorder , 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 &
mood.
 There is degeneration of brain neurons
especially in the cerebral cortex and presence
of neurofibrillary tangles and plaques
containing beta-amyloid cells

3. 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

4. Definitions
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.

5. COMPARISON OF A NORMAL AGED BRAIN
(LEFT) AND AN ALZHEIMER'S PATIENT'S BRAIN
(RIGHT). DIFFERENTIAL CHARACTERISTICS
ARE POINTED OUT.

6. BRAIN CROSS SECTIONS
FIGURE –2 NEUROBIOLOGY OF ALZHEIMER’S
DISEASE.
Gyrus
Normal Alzheimer’s
Memory
Memory
LanguageLanguage
Ventricle
Gyrus
Sulcus
Sulcus

7. 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.

8. PREVALENCE

9. CAUSES
The cause of Alzheimer’s disease is
not known.
However, several factors on the basis
of hypothesis are thought to be implicated
in this disease.

10. 1.NEUROCHEMICALFACTORS
a) Acetylcholine alteration
b) Others: serotonin, dopamine, nor epinephrine
c) Amino acid glutamate: excess glutamate
leads to overstimulation of the N-methyl-D-
aspartate (NMDA) receptors, leading to
increased intracellular calcium, and
subsequent neuronal degeneration and cell
death.
d) Somatostatin.
e) Substance P.

11. 2. Plaques and Tangles.
 An overabundance of structures called
plaques and tangles appears in the
brains of individuals with AD.
 The plaques are made of a protein
called amyloid beta (Aβ ), which are
fragments of a larger protein called
amyloid precursor protein.
 Plaques are formed when these
fragments clump together and mix with
molecules and other cellular matter.
 Tangles are formed from a special kind
of cellular protein called tau protein,
whose function it is to provide stability to
the neuron.
 In AD, the tau protein is chemically
altered).
 Strands of the protein become tangled
together, interfering with the neuronal
transport system.

12. 3.Head Trauma:
 The etiology of AD has been associated with
serious head trauma.
 Studies have shown that some individuals who had
experienced head trauma had subsequently (after
years) developed AD.
 Munoz and Feldman (2000) report an increased risk
for AD in individuals who are both genetically
predisposed and who experience traumatic head
injury.

13. 4.Genetic Factors:
There is clearly a familial pattern with some forms
of AD.
 Some families exhibit a pattern of inheritance that
suggests possible autosomal dominant gene
transmission.
 People with Down syndrome, who carry an extra
copy of chromosome 21, have been found to be
unusually susceptible to AD

14. 5.ENVIRONMENTAL FACTORS:
• Cigarette smoking.
• Certain Infections.
• Metals, industrial or other toxins.
• Use of cholesterol lowering drugs
(statin).

15. RISK FACTORS
1.Increased age(over 65 years of age)
2. Females
3. Hypertension
4. Increased cholesterol level
5.Coronary artery disease
6. Diabetes
7. Mild cognitive decline

16. 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.

17. 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

18. Microscopy image of a neurofibrillary tangle,
conformed by hyperphosphorylated tau
protein

20. • 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

21. In Alzheimer's disease, changes in tau protein lead to the
disintegration of microtubules in brain cells.

22. SIGNS
Ten warning signs of Alzheimer's disease
1) Memory loss
2) Difficulty to performing familiar tasks
3) Problems with language
4) Disorientation to time and place
5) Poor or decreased judgment
6) Problems with abstract thinking
7) Misplacing things
8) Changes in mood or behavior
9) Changes in personality
10) Loss of initiative

23. SYMPTOMS
• Confusion
• disturbances in short-term memory
• problems with attention and spatial orientation
• personality changes
• language difficulties
• unexplained mood swings

24. COGNITIVE DISTURBANCES

25. DIAGNOSTIC TESTS
• Psychiatric assessments.
• Mental status examination and
assessment.
• Laboratory tests.
• Brain imaging .
* CT scan
* MRI
* PET
* SPECT
• CSF Examination
neuro psychological
• Electro-encephalogram (EEG)
• Electromyogram

26. PET scan of the brain of a person with AD showing
a loss of function in the temporal lobe

27. INTERVENTIONS

28. PHARMACOLOGICAL INTERVENTION
• Acetylcholinesterase inhibitors -prevent the
breakdown of acetylcholine, a chemical
messenger important for learning and memory
eg. Donepezil (Aricept)
Rivastigmine (Exelon)
Galantamine (Razadyne

29. N-Methyl d-aspartate Receptor Antagonist
(NMDA)
• Eg:Memantine – blocks the NMDA
receptor and inhibit their overstimulation
by glutamate (neurotransmitter)
• Antidepressents.
• Anxiolytics.
• Antipsychotics.
• Anticonvulsants

30. PSYCHOSOCIAL INTERVENTION
 Behavioral approach
 Emotion oriented approach
 Remnisence therapy
 Validation therapy
 supportive psychotherapy
 sensory integration(multisensory tool
stimulate the users by providing exciting
visuals, music, sounds
aromas and texture to explore)
 stimulated presence therapy
• Cognition oriented approach
• Stimulation oriented approach
snoezelen;

31. 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

32. 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.

33. • 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.