2. CASE STUDY
Allie, a 72 year old lady was brought to see a
neuropsychologist for an evaluation of memory loss
of a progressive nature. The symptoms had been
present for years and were getting worse. Her
memory loss originally took the form of a tendency
to repeat questions and ideas. As the symptoms
progressed, her son, reported that her mother was
having trouble reasoning and was disoriented with
regards to time, day, month and year. Frequently,
Allie did not understand were she was when outside
of home.

3. CASE STUDY
Her son described that his mother is still
experiencing anxiety and depression, which was
signified a personality change in her mother despite
multiple courses of medication for depression. She
is now also tended to be overall aggressive towards
others, which was not her usual manner. In
addition, her son reported that his mother had
begun to require supervision in dressing, bathing,
and grooming and required reminders to change
his clothes. Frequently, Allie would wear the same
clothes repeatedly. It was also noted that she had
become socially withdrawn.

4. CASE STUDY
During the doctor’s evaluation, she was very
upset when she was examined, because she did
not comprehend why she was there.
Throughout the visit, she had difficulty finding
words. Even without any other medical or
neurological evaluations, all these indications
made it obvious to the neuropsychologist that
she had classic Alzheimer’s disease in the
moderately severe stages.

5. ALZHEIMER’S DISEASE
Severe type of mental Prognosis for patient is
deterioration, or poor. (2007, Lippincot
dementia, usually Williams & Wilkins)
affects older people.
(2007, Seeley et. Al,
Essentials of Anatomy Causes gradual memory loss, decline
in the ability to perform routine tasks,
and Physiology)
disorientation, difficulty in learning,
loss of language skills, impairment of
Progressive,
judgement and personality changes.
degenerative brain ( 2008, Sabbagh, The Alzheimer’s
disease that impairs Answer)
memory, thinking, and
behaviour. (2007,
Lippincot Williams &
Wilkins)
NO ONE IS IMMUNED

6. ALZHEIMER’S DISEASE
1906:
Dr. Alois Alzheimer
first described the
disease.
1974:
Founding of National
Institute on Aging
1980:
Alzheimer’s Association founded.
Jerome H. Stone is the President.

7. ALZHEIMER’S DISEASE
1993:
Tacrine (Cognex)- First
Alzheimer Drug
approved by FDA.
2000:
Alzheimer’s Disease
Association of the
Philippines was
founded.
2011:
President Obama signs National
Alzheimer’s Project Act (NAPA) into
law.

8. 1994:
Ronald Reagan’s
Alzheimer’s Disease
diagnosis announced.

9. STAGES OF AD:
1. PRE-CLINICAL ALZHEIMER’S DISEASE
-Begins near the hippocampus (structure
essential to formation of both short & longterm
memories)
-Affected region begins to shrink.

10. STAGES OF AD:
2. MILD ALZHEIMER’S DISEASE
-Cerebral cortex begins to shrink.
-Memory disturbance usually noticed.
-Poor judgement and problem-solving skills,
careless in work and household.
-Irritable, suspicious or indifferent.
-Cognitive impairments: Agitation, apathy,
dysphoria and aberrant motor behaviour.

11. STAGES OF AD:
3. MODERATE ALZHEIMER’S DISEASE
-Client demonstrate Language disturbance,
characterized by impaired word-finding and
circumlocution (talking around subject rather
than about it directly)
-Paraphasias (words used in the wrong context)
-Apraxia (motor disturbance)
-Hyperorality (desire to take everything into the
mouth to chew, suck or taste)

12. STAGES OF AD:
4. SEVERE ALZHEIMER’S DISEASE
-Plaques and tangles are widespread throughout
the brain.
-Clients can’t recognize family and loved ones.
-Voluntary movement is minimal, limbs are rigid
with flexor posturing.
-Aspiration pneumonia is common.

14. LOCAL STATISTICS
7,900 patients were
hospitalized with initial
diagnosis of Alzheimer’s
disease. ( Hospital Episode
Statistics, DOH, 2000)

15. GLOBAL STATISTICS

16. PATHOPHYSIOLOGY

17. 3 HALLMARKS OF AD:
1. Beta-amyloid plaques
- Composed of degenerating axons and
dendrites.
- Dense deposits of protein & cellular material
that accumulate outside & around nerve
cells.

18. Beta-amyloid Plaques
Amyloid precursor protein (APP) is
the precursor to amyloid plaque.
1.
1. APP sticks through the neuron
membrane.
2. Enzymes cut the APP into
fragments of protein, including beta-
amyloid.
3. Beta-amyloid fragments come 2.
together in clumps to form plaques.
In AD, many of these clumps form, disrupting
the work of neurons. This affects the
hippocampus and other areas of the cerebral
cortex. 3.

19. 3 HALLMARKS OF AD:
2. Neurofibrillatory Tangles
-Fibrous proteins
-Twisted fibers that build up inside the nerve
cells.

20. Neurofibrillatory Tangles

21. 3 HALLMARKS OF AD:
3. Neuronal Cell Death
Composed of degenerating axons and dendrites.
-Dense deposits of protein & cellular material
that accumulate outside & around nerve cells.

25. CLINICAL MANIFESTATIONS
Presence of β-amyloid plaques
neurofibrillary tangles in and neuronal
cell death in:
Frontal Lobe Temporal Lobe Parietal Lobe Occipital Lobe
(includes the
hippocampus)
- challenges in - impaired personal - Trouble
planning -memory care skills understanding visual
- impairment in disturbance/ images and spatial
mental flexibility and impairment relationships
spontaneity (difficulty in -impairment of visual
-socialization is remembering short- memories
impaired term memory) ;
- low problem - reduced inhibition
solving skills of talking
-agitation -difficulty in
recognizing words
-difficulty in
remembering verbal
material

26. LATEST RESEARCH REGARDING AD:

27. Medscape Medical News reported on the latest published
research in Alzheimer’s disease on November 7, 2012 indicating
individuals carrying a mutant gene for Alzheimer’s disease
demonstrate markers 20 years before onset of memory changes.
In addition to markers in the cerebral spinal fluid, the individuals
show structural changes in the brain other than the amyloid
plaques and tangles commonly found in patients with the disease.
Dr. Eric M. Reiman, the first author on this recent study,
published his results in Lancet Neurology on November 6, 2012.
His research group from the Banner Alzheimer’s Institute in
Phoenix, Arizona studied about 5000 people who carry the gene
mutation that produces Alzheimer’s disease as early as age 45
years in Colombia.

28. Reiman and colleagues compared carriers of the gene with non-carriers
and found structural differences in area of the brain called the
hippocampus as well as less grey matter in some parietal lobes in
individuals with the Alzheimer’s gene mutation. The parietal lobe
resides at the top of the head after the frontal lobe and before the
occipital lobe at the back of the head. The researchers used magnetic
resonance imaging to uncover the changes in the parietal lobe. These
changes occurred 20 years before the onset of memory loss. By
knowing these alterations exist early, researchers can study treatments
and measure for differences at these sites.
According to the Center for Disease Control and Prevention,
Alzheimer’s disease causes the most common form of dementia that
produces loss of thought control, memory and language. The disease
usually affects men and women over the age of 60 years. The cause of
Alzheimer’s disease remains presently unknown. Most scientists think
several factors such as genetic, environmental and lifestyle contribute
to the development of the disease. The discovery of changes in the
parietal lobe and hippocampus add significantly to progress in the
research.

29. The National Institute on Aging describes the
importance of clinical research for uncovering causes,
treatment modalities and disease prevention in
Alzheimer’s disease. Patients or families interested in
becoming involved in research trials can go the Clinical
Trials.gov website for more information. The research
trial website lists trials available in all 50 states and 181
countries.
Source: http://www.examiner.com/article/remarkable-
recent-discoveries-alzheimer-s-disease

30. PHARMACOLOGY

31. Research Topic
• Alzheimer’s disease: Abstainers or binge
drinkers. Who are the most at risk population?

32. Treatment
1. Patient & Family education regarding memory
aids, diet, and safety issues may slow the
progression of symptoms.
2. Medications:
•Namenda
•Razadyne
•Exelon
•Aricept

33. Treatment
3. Cholinesterase inhibitors
-Donezepil
-Rivastigmine
-Galantamine
4. Vitamin E- may slow progression of death,
institutionalization and severe AD

34. Ethical Considerations
Ethical Issues in the Early Diagnosis of Alzheimer Disease
Matthew E. Growdon
Mattsson N, Brax D, Zetterberg H. To know or not to know: ethical issues related to early diagnosis of
Alzheimer’s disease. Int J Alzheimers Dis. 2010.
While a disease-modifying treatment for Alzheimer disease (AD) remains elusive, recent advances have shed light
on its pathophysiology, giving patients and researchers alike hope that a viable treatment will emerge. Research
efforts have identified promising drug targets for clinical trials and uncovered cerebrospinal fluid (CSF) biomarkers
and imaging studies that allow for preclinical detection of AD pathology. The recognition that the hallmark plaques
and tangles of AD are detectable in the brains of individuals more then 10 years before they present with any
cognitive changes underscored the need to validate biomarkers that could reliably detect AD and chart its
progression.
In April 2011, the Alzheimer’s Association [1] updated the criteria for the diagnosis of Alzheimer’s disease
dementia for the first time in 27 years. Their report emphasizes biomarker data and lays out research guidelines
for the preclinical diagnosis of AD meant to facilitate ongoing clinical research and drug discovery efforts [2].
Implicit in these new guidelines is the hope that effective therapies are around the corner and the belief that
interventions should be designed for individuals before their brains are irreversibly damaged. The well-placed
optimism of scientific progress can obscure the humanistic dimensions of early diagnosis. In “To Know or Not to
Know: Ethical Issues Related to Early Diagnosis of Alzheimer’s Disease,” Niklas Mattsson, David Brax, and Henrik
Zetterberg examine the ethical issues surrounding the early diagnosis of AD. They emphasize the potentially
harmful consequences of early diagnosis to the patient and raise important questions about personal identity and
decision-making competence that are central to the diagnosis and management of AD. Their article is a timely
reminder about the powerful, life-altering effects of diagnosis and, above all, the enduring need to place the
patient’s desires and preferences at the center of the clinical encounter.
As a point of departure, Mattsson et al. consider the potential for misdiagnosis of AD, even in the era of
sophisticated biomarker studies. Several studies underscore the high diagnostic accuracy of cerebrospinal fluid
(CSF) biomarkers, with sensitivity and specificity around 85-90 percent in identifying incipient AD in patients
diagnosed with mild cognitive impairment, an intermediate stage between the expected cognitive decline of
normal aging and the pronounced decline of dementia [3].
However, the authors acknowledge the enduring possibility of misdiagnosis in populations or samples in which
there is a low prevalence of disease because of false positive screening results. Furthermore, while severe
complications are rare, lumbar punctures to obtain CSF are associated with post-LP headaches in 2-4 percent of
patients [4]. Colloquially referred to as “spinal taps,” lumbar punctures are feared by many patients, to the point
that there have been calls within professional circles to rename the procedure and move it into the mainstream of
clinical practice in dementia care [5].

35. Nursing Care Plan
Nursing diagnosis/problem:
Altered cognitive and perceptual abilities
related to loss of nerve cells
Goal: Provide safe, structured environment

36. Nursing Interventions Rationale Outcome Criteria
1. Place patient in location 1. The patient with AD is easily 1. Patient will remain safe and
where observation is easy confused by new relatively stable.
(near nurses’ station, with surroundings.
reliable roommate, or where
family can stay)
2. Establish and maintain 2. The ability to adjust to a new
consistent environment, environment and learn new
including staff personnel. material is severely limited.
3. Remove all potentially 3. .
dangerous objects (e.g., razor,
scissors, matches
4. Approach patient in calm, 4. The behavior of others is
unhurried, firm but tolerant mirrored in the patient’s
manner. behavior.

37. References:
• Black, J. (2008). Medical-Surgical Nursing 8th Edition. Singapore: Elsevier Pte. Ltd
• Morrison A., Lykestos C. (2005). The Pathophysiology of Alzheimer’s Disease and Directions in
Treatment. Galen Publishing LLC.
• http://www.buzzle.com/articles/lobes-of-the-brain-and-their-function.html
• Black, J (2008). Medical-Surgical Nursing 8th Edition. pp. 1746-1747
• Sabbagh, M.D., M (2008). The Alzheimer’s Answer
• http://www.examiner.com/article/remarkable-recent-discoveries-alzheimer-s-disease