Contents

1. Alzheimer’s Disease …………………………………………………………2

2. Signs and Symptoms………………………………………………………4
3. Causes……………………………………………………………………………6
4. Pathophysiology……………………………………………………………8
5. Diagnosis………………………………………………………………………12
6. Prevention……………………………………………………………………18
7. Management ……………………………………………………………..23
8. History………………………………………………………………………28
9. Bibliography…………………………………………………………….31

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1. Alzheimer’s Disease
Alzheimer's disease (AD) is a neurodegenerative disease that
usually starts slowly and progressively worsens, and is the
cause of 60–70% of cases of dementia. The most common
early symptom is difficulty in remembering recent events. As
the disease advances, symptoms can include problems with
language, disorientation (including easily getting lost), mood
swings, loss of motivation, self-neglect, and behavioral
issues. As a person's condition declines, they often withdraw
from family and society. Gradually, bodily functions are lost,
ultimately leading to death. Although the speed of
progression can vary, the typical life expectancy following
diagnosis is three to nine years.

The cause of Alzheimer's disease is poorly understood. There

are many environmental and genetic risk factors associated
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with its development. The strongest genetic risk factor is
from an allele of APOE. Other risk factors include a history of
head injury, clinical depression, and high blood pressure. The
disease process is largely associated with amyloid plaques,
neurofibrillary tangles, and loss of neuronal connections in
the brain. A probable diagnosis is based on the history of the
illness and cognitive testing, with medical imaging and blood
tests to rule out other possible causes. Initial symptoms are
often mistaken for normal brain aging. Examination of brain
tissue is needed for a definite diagnosis, but this can only
take place after death. Good nutrition, physical activity, and
engaging socially are known to be of benefit generally in
aging, and may help in reducing the risk of cognitive decline
and Alzheimer's.

No treatments can stop or reverse its progression, though

some may temporarily improve symptoms. Affected people
become increasingly reliant on others for assistance, often
placing a burden on caregivers.

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2. Signs and Symptoms
Changes in mood and behavior sometimes happen even
before memory problems occur. Symptoms get worse over
time. Eventually, most people with dementia will need others
to help with daily activities.

Early signs and symptoms are:

 Forgetting things or recent events

 Losing or misplacing things
 Getting lost when walking or driving
 Being confused, even in familiar places
 Losing track of time
 Difficulties solving problems or making decisions
 Problems following conversations or trouble finding
words

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  Difficulties performing familiar tasks
 Misjudging distances to objects visually.
Common changes in mood and behavior include:

 Feeling anxious, sad, or angry about memory loss

 Personality changes
 Inappropriate behavior
 Withdrawal from work or social activities
 Being less interested in other people’s emotions.
Dementia affects each person in a different way, depending
upon the underlying causes, other health conditions and the
person’s cognitive functioning before becoming ill.

Most symptoms become worse over time, while others might

disappear or only occur in the later stages of dementia. As
the disease progresses, the need for help with personal care
increases. People with dementia may not be able to
recognize family members or friends, develop difficulties
moving around, lose control over their bladder and bowls,
have trouble eating and drinking and experience behavior
changes such as aggression that are distressing to the person
with dementia as well as those around them.

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3. Causes
There are 3 main causes for Alzheimer’s disease:
1. Age
The greatest known risk factor for Alzheimer’s and
other dementias is increasing age, but these disorders
are not a normal part of aging. While age increases risk,
it is not a direct cause of Alzheimer's.

Most individuals with the disease are 65 and older. After

age 65, the risk of Alzheimer's doubles every five years.
After age 85, the risk reaches nearly one-third.

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2. Family History
Another strong risk factor is family history. Those who
have a parent, brother or sister with Alzheimer’s are more
likely to develop the disease. The risk increases if more
than one family member has the illness. When diseases
tend to run in families, either heredity (genetics),
environmental factors, or both, may play a role.
3. Genetics
Scientists know genes are involved in Alzheimer’s. Two
categories of genes influence whether a person
develops a disease: risk genes and deterministic genes.
Alzheimer's genes have been found in both categories.
It is estimated that less than 1% of Alzheimer’s cases
are caused by deterministic genes (genes that cause a
disease, rather than increase the risk of developing a
disease).

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4.Pathophysiology
 Neuropathy
Alzheimer's disease is characterized by loss of neurons and
synapses in the cerebral cortex and certain subcortical regions.
This loss results in gross atrophy of the affected regions,
including degeneration in the temporal lobe and parietal lobe,
and parts of the frontal cortex and cingulate gyrus.
Degeneration is also present in brainstem nuclei particularly the
locus coeruleus in the pons. Studies using MRI and PET have
documented reductions in the size of specific brain regions in
people with Alzheimer's disease as they progressed from mild
cognitive impairment to Alzheimer's disease, and in comparison
with similar images from healthy older adults.

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Both Aβ plaques and neurofibrillary tangles are clearly visible
by microscopy in brains of those with Alzheimer's disease,
especially in the hippocampus. However, Alzheimer's disease
may occur without neurofibrillary tangles in the neocortex.
Plaques are dense, mostly insoluble deposits of beta-amyloid
peptide and cellular material outside and around neurons.
Tangles (neurofibrillary tangles) are aggregates of the
microtubule-associated protein tau which has become hyper
phosphorylated and accumulate inside the cells themselves.
Although many older individuals develop some plaques and
tangles as a consequence of aging, the brains of people with
Alzheimer's disease have a greater number of them in specific
brain regions such as the temporal lobe. Lewy bodies are not
rare in the brains of people with Alzheimer's disease.

 Biochemistry
Alzheimer's disease has been identified as a protein misfolding
disease, a proteopathy, caused by the accumulation of
abnormally folded amyloid beta protein into amyloid plaques,
and tau protein into neurofibrillary tangles in the brain. Plaques
are made up of small peptides, 39–43 amino acids in length,
called amyloid beta (Aβ). Amyloid beta is a fragment from the
larger amyloid-beta precursor protein (APP) a trans membrane
protein that penetrates the neuron's membrane. APP is critical
to neuron growth, survival, and post-injury repair. In
Alzheimer's disease, gamma secretase and beta secretase act

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together in a proteolytic process which causes APP to be
divided into smaller fragments. One of these fragments gives
rise to fibrils of amyloid beta, which then form clumps that
deposit outside neurons in dense formations known as amyloid
plaques.

Alzheimer's disease is also considered a tauopathy due to

abnormal aggregation of the tau protein. Every neuron has a
cytoskeleton, an internal support structure partly made up of
structures called microtubules. These microtubules act like
tracks, guiding nutrients and molecules from the body of the
cell to the ends of the axon and back. A protein called tau
stabilizes the microtubules when phosphorylated, and is
therefore called a microtubule-associated protein. In
Alzheimer's disease, that undergoes chemical changes,
becoming hyper phosphorylated; it then begins to pair with
other threads, creating neurofibrillary tangles and
disintegrating the neuron's transport system. Pathogenic tau
can also cause neuronal death through transposable element
dysregulation. Necroptosis has also been reported as a
mechanism of cell death in brain cells affected with tau tangles.

 Disease Mechanism
Exactly how disturbances of production and
aggregation of the beta-amyloid peptide give rise to
the pathology of Alzheimer's disease is not known.
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 The amyloid hypothesis traditionally points to the
accumulation of beta-amyloid peptides as the central
event triggering neuron degeneration. Accumulation
of aggregated amyloid fibrils, which are believed to
be the toxic form of the protein responsible for
disrupting the cell's calcium ion homeostasis, induces
programmed cell death (apoptosis). It is also known
that Aβ selectively builds up in the mitochondria in
the cells of Alzheimer's-affected brains, and it also
inhibits certain enzyme functions and the utilization
of glucose by neurons.

Iron dyshomeostasis is linked to disease progression, an iron-

dependent form of regulated cell death called Ferroptosis could
be involved. Products of lipid peroxidation are also elevated in
AD brain compared with controls.

Various inflammatory processes and cytokines may also have a

role in the pathology of Alzheimer's disease. Inflammation is a
general marker of tissue damage in any disease, and may be
either secondary to tissue damage in Alzheimer's disease or a
marker of an immunological response. There is increasing
evidence of a strong interaction between the neurons and the
immunological mechanisms in the brain. Obesity and systemic
inflammation may interfere with immunological processes
which promote disease progression.
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Alterations in the distribution of different neurotropic factors
and in the expression of their receptors such as the brain-
derived neurotropic factor (BDNF) have been described in
Alzheimer's disease.

5.Diagonosis
Alzheimer's disease (AD) can only be definitively diagnosed with
autopsy findings; in the absence of autopsy, clinical diagnoses
of AD are "possible" or "probable", based on other findings. Up
to 23% of those clinically diagnosed with AD may be
misdiagnosed and may have pathology suggestive of another
condition with symptoms that mimic those of AD.
AD is usually clinically diagnosed based on the person's medical
history, history from relatives, and behavioral observations. The
presence of characteristic neurological and neuropsychological
features and the absence of alternative conditions supports the
diagnosis. Advanced medical imaging with computed
tomography (CT) or magnetic resonance imaging (MRI), and
with single-photon emission computed tomography (SPECT) or
positron emission tomography (PET), can be used to help
exclude other cerebral pathology or subtypes of dementia.
Moreover, it may predict conversion from prodromal stages
(mild cognitive impairment) to Alzheimer's disease. FDA-
approved radiopharmaceutical diagnostic agents used in PET

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for Alzheimer's disease are florbetapir (2012), flutemetamol
(2013), florbetaben (2014), and flortaucipir (2020).Because
many insurance companies in the United States do not cover
this procedure, its use in clinical practice is largely limited to
clinical trials as of 2018.

Assessment of intellectual functioning including memory

testing can further characterize the state of the disease.
Medical organizations have created diagnostic criteria to ease
and standardize the diagnostic process for practicing
physicians. Definitive diagnosis can only be confirmed with
post-mortem evaluations when brain material is available and
can be examined histologically for senile plaques and
neurofibrillary tangles.

Criteria
There are three sets of criteria for the clinical diagnoses of the
spectrum of Alzheimer's disease: the 2013 fifth edition of the
Diagnostic and Statistical Manual of Mental Disorders (DSM-5);
the National Institute on Aging-Alzheimer's Association (NIA-
AA) definition as revised in 2011; and the International Working
Group criteria as revised in 2010. Three broad time periods,
which can span decades, define the progression of Alzheimer's
disease from the preclinical phase, to mild cognitive
impairment (MCI), followed by Alzheimer's disease dementia.

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Eight intellectual domains are most commonly impaired in AD
—memory, language, perceptual skills, attention, motor skills,
orientation, problem solving and executive functional abilities,
as listed in the fourth text revision of the DSM (DSM-IV-TR).

The DSM-5 defines criteria for probable or possible Alzheimer's

for both major and mild neurocognitive disorder. Major or mild
neurocognitive disorder must be present along with at least
one cognitive deficit for a diagnosis of either probable or
possible AD. For major neurocognitive disorder due to
Alzheimer's disease, probable Alzheimer's disease can be
diagnosed if the individual has genetic evidence of Alzheimer's
or if two or more acquired cognitive deficits, and a functional
disability that is not from another disorder, are present.
Otherwise, possible Alzheimer's disease can be diagnosed as
the diagnosis follows an atypical route. For mild neurocognitive
disorder due to Alzheimer's, probable Alzheimer's disease can
be diagnosed if there is genetic evidence, whereas possible
Alzheimer's disease can be met if all of the following are
present: no genetic evidence, decline in both learning and
memory, two or more cognitive deficits, and a functional
disability not from another disorder.

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The NIA-AA criteria are used mainly in research rather than in
clinical assessments. They define Alzheimer's disease through
three major stages: preclinical, mild cognitive impairment
(MCI), and Alzheimer's dementia. Diagnosis in the preclinical
stage is complex and focuses on asymptomatic individuals; the
latter two stages describe individuals experiencing symptoms.
The core clinical criteria for MCI is used along with
identification of biomarkers, predominantly those for neuronal
injury (mainly tau-related) and amyloid beta deposition.The
core clinical criteria itself rests on the presence of cognitive
impairment without the presence of comorbidities. The third
stage is divided into probable and possible Alzheimer's disease
dementia. In probable Alzheimer's disease dementia there is
steady impairment of cognition over time and a memory-
related or non-memory-related cognitive dysfunction. In
possible Alzheimer's disease dementia, another causal disease
such as cerebrovascular disease is present.

 Techniques
Neuropsychological tests including cognitive tests such
as the mini–mental state examination (MMSE), the
Montreal Cognitive Assessment (MoCA) and the Mini-
Cog are widely used to aid in diagnosis of the cognitive
impairments in AD. These tests may not always be
accurate, as they lack sensitivity to mild cognitive
impairment, and can be biased by language or attention
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 problems; more comprehensive test arrays are
necessary for high reliability of results, particularly in
the earliest stages of the disease.

Further neurological examinations are crucial in the differential

diagnosis of Alzheimer's disease and other diseases. Interviews
with family members are used in assessment; caregivers can
supply important information on daily living abilities and on the
decrease in the person's mental function. A caregiver's
viewpoint is particularly important, since a person with
Alzheimer's disease is commonly unaware of their deficits.
Many times, families have difficulties in the detection of initial
dementia symptoms and may not communicate accurate
information to a physician.

Supplemental testing can rule out other potentially treatable

diagnoses and help avoid misdiagnoses. Common supplemental
tests include blood tests, thyroid function tests, as well as tests
to assess vitamin B12 levels, rule out neurosyphilis and rule out
metabolic problems (including tests for kidney function,
electrolyte levels and for diabetes). MRI or CT scans might also
be used to rule out other potential causes of the symptoms –
including tumors or strokes.Delirium and depression can be
common among individuals and are important to rule out.

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Psychological tests for depression are used, since depression
can either be concurrent with Alzheimer's disease (see
Depression of Alzheimer disease), an early sign of cognitive
impairment, or even the cause.
Due to low accuracy, the C-PIB-PET scan is not recommended
as an early diagnostic tool or for predicting the development of
Alzheimer's disease when people show signs of mild cognitive
impairment (MCI). The use of 18F-FDG PET scans, as a single
test, to identify people who may develop Alzheimer's disease is
not supported by Experiment.

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6.Prevention
There are no disease-modifying treatments available to cure
Alzheimer's disease and because of this, AD research has
focused on interventions to prevent the onset and progression.
There is no evidence that supports any particular measure in
preventing Alzheimer's, and studies of measures to prevent the
onset or progression have produced inconsistent results.
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Epidemiological studies have proposed relationships between
an individual's likelihood of developing AD and modifiable
factors, such as medications, lifestyle, and diet. There are some
challenges in determining whether interventions for
Alzheimer's disease act as a primary prevention method,
preventing the disease itself, or a secondary prevention
method, identifying the early stages of the disease. These
challenges include duration of intervention, different stages of
disease at which intervention begins, and lack of
standardization of inclusion criteria regarding biomarkers
specific for Alzheimer's disease.Further research is needed to
determine factors that can help prevent Alzheimer's disease.

 Medication
Cardiovascular risk factors, such as hypercholesterolaemia,
hypertension, diabetes, and smoking, are associated with a
higher risk of onset and worsened course of AD. The use of
statins to lower cholesterol may be of benefit in Alzheimer's.
Antihypertensive and antidiabetic medications in individuals
without overt cognitive impairment may decrease the risk of
dementia by influencing cerebrovascular pathology. More
research is needed to examine the relationship with
Alzheimer's disease specifically; clarification of the direct role
medications play versus other concurrent lifestyle changes
(diet, exercise, smoking) is needed.

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Depression is associated with an increased risk for Alzheimer's
disease; management with antidepressants may provide a
preventative measure.

Historically, long-term usage of non-steroidal anti-inflammatory

drugs (NSAIDs) were thought to be associated with a reduced
likelihood of developing Alzheimer's disease as it reduces
inflammation; however, NSAIDs do not appear to be useful as a
treatment. Additionally, because women have a higher
incidence of Alzheimer's disease than men, it was once thought
that estrogen deficiency during menopause was a risk factor.
However, there is a lack of evidence to show that hormone
replacement therapy (HRT) in menopause decreases risk of
cognitive decline.Plant-made metallochaperones could be a
novel approach for the treatment of Alzheimer's disease.

 Lifestyle
Certain lifestyle activities, such as physical and cognitive
exercises, higher education and occupational attainment,
cigarette smoking, stress, sleep, and the management of other
comorbidities, including diabetes and hypertension, may affect
the risk of developing Alzheimer's.

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Physical exercise is associated with a decreased rate of
dementia, and is effective in reducing symptom severity in
those with AD. Memory and cognitive functions can be
improved with aerobic exercises including brisk walking three
times weekly for forty minutes.It may also induce
neuroplasticity of the brain. Participating in mental exercises,
such as reading, crossword puzzles, and chess have shown a
potential to be preventative. Meeting the WHO
recommendations for physical activity is associated with a
lower risk of AD.

Higher education and occupational attainment, and

participation in leisure activities, contribute to a reduced risk of
developing Alzheimer's, or of delaying the onset of symptoms.
This is compatible with the cognitive reserve theory, which
states that some life experiences result in more efficient neural
functioning providing the individual a cognitive reserve that
delays the onset of dementia manifestations.Education delays
the onset of Alzheimer's disease syndrome without changing
the duration of the disease.

Cessation in smoking may reduce risk of developing

Alzheimer's' disease, specifically in those who carry APOE ɛ4
allele. The increased oxidative stress caused by smoking results
in downstream inflammatory or neurodegenerative processes
that may increase risk of developing AD. Avoidance of smoking,
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counseling and pharmacotherapies to quit smoking are used,
and avoidance of environmental tobacco smoke is
recommended.

Alzheimer's disease is associated with sleep disorders but the

precise relationship is unclear. It was once thought that as
people get older, the risk of developing sleep disorders and AD
independently increase, but research is examining whether
sleep disorders may increase the prevalence of AD. One theory
is that the mechanisms to increase clearance of toxic
substances, including Aβ, are active during sleep. With
decreased sleep, a person is increasing Aβ production and
decreasing Aβ clearance, resulting in Aβ accumulation.
Receiving adequate sleep (approximately 7–8 hours) every
night has become a potential lifestyle intervention to prevent
the development of AD.
Stress is a risk factor for the development of Alzheimer’s. The
mechanism by which stress predisposes someone to
development of Alzheimer's is unclear, but it is suggested that
lifetime stressors may affect a person's epigenome, leading to
an overexpression or under expression of specific genes.
Although the relationship of stress and Alzheimer's is unclear,
strategies to reduce stress and relax the mind may be helpful
strategies in preventing the progression or Alzheimer's disease.
Meditation, for instance, is a helpful lifestyle change to support

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cognition and well-being, though further research is needed to
assess long-term effects.

7.Management
There is no cure for Alzheimer's disease; available treatments
offer relatively small symptomatic benefits but remain palliative
in nature. Treatments can be divided into pharmaceutical,
psychosocial, and caregiving.
 Pharmaceutical
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Medications used to treat the cognitive symptons of
Alzheimer's disease rather than the underlying cause include:
four acetylcholinesterase inhibitors (tacrine, rivastigmine,
galantamine, and donepezil) and memantine, an NMDA
receptor antagonist. The acetylcholinesterase inhibitors are
intended for those with mild to severe Alzheimer's, whereas
memantine is intended for those with moderate or severe
Alzheimer's disease. The benefit from their use is small.

Reduction in the activity of the cholinergic neurons is a well-

known feature of Alzheimer's disease. Acetylcholinesterase
inhibitors are employed to reduce the rate at which
acetylcholine (ACh) is broken down, thereby increasing the
concentration of ACh in the brain and combating the loss of
ACh caused by the death of cholinergic neurons.There is
evidence for the efficacy of these medications in mild to
moderate Alzheimer's disease, and some evidence for their use
in the advanced stage. The use of these drugs in mild cognitive
impairment has not shown any effect in a delay of the onset of
Alzheimer's disease. The most common side effects are nausea
and vomiting, both of which are linked to cholinergic excess.
These side effects arise in approximately 10–20% of users, are
mild to moderate in severity, and can be managed by slowly
adjusting medication doses. Less common secondary effects
include muscle cramps, decreased heart rate (bradycardia),

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decreased appetite and weight, and increased gastric acid
production.

Glutamate is an excitatory neurotransmitter of the nervous

system, although excessive amounts in the brain can lead to
cell death through a process called excitotoxicity which consists
of the overstimulation of glutamate receptors. Excitotoxicity
occurs not only in Alzheimer's disease, but also in other
neurological diseases such as Parkinson's disease and multiple
sclerosis. Memantine is a noncompetitive NMDA receptor
antagonist first used as an anti-influenza agent. It acts on the
glutamatergic system by blocking NMDA receptors and
inhibiting their overstimulation by glutamate. Memantine has
been shown to have a small benefit in the treatment of
moderate to severe Alzheimer's disease. Reported adverse
events with memantine are infrequent and mild, including
hallucinations, confusion, dizziness, headache and fatigue. The
combination of memantine and donepezil has been shown to
be "of statistically significant but clinically marginal
effectiveness".

An extract of Ginkgo biloba known as EGb 761 has been used

for treating Alzheimer's and other neuropsychiatric disorders.
Its use is approved throughout Europe. The World Federation
of Biological Psychiatry guidelines lists EGb 761 with the same
weight of evidence (level B) given to acetylcholinesterase
25
inhibitors and memantine. EGb 761 is the only one that showed
improvement of symptoms in both Alzheimer's disease and
vascular dementia. EGb 761 may have a role either on its own
or as an add-on if other therapies prove ineffective. A 2016
review concluded that the quality of evidence from clinical
trials on Ginkgo biloba has been insufficient to warrant its use
for treating Alzheimer's disease.

Atypical antipsychotics are modestly useful in reducing

aggression and psychosis in people with Alzheimer's disease,
but their advantages are offset by serious adverse effects, such
as stroke, movement difficulties or cognitive decline. When
used in the long-term, they have been shown to associate with
increased mortality. Stopping antipsychotic use in this group of
people appears to be safe.
 Psychological
Psychosocial interventions are used as an adjunct to
pharmaceutical treatment and can be classified within
behavior-, emotion-, cognition- or stimulation-oriented
approaches.

Behavioral interventions attempt to identify and reduce the

antecedents and consequences of problem behaviors. This
approach has not shown success in improving overall
functioning, but can help to reduce some specific problem
26
behaviors, such as incontinence. There is a lack of high quality
data on the effectiveness of these techniques in other behavior
problems such as wandering. Music therapy is effective in
reducing behavioral and psychological symptoms.

Emotion-oriented interventions include reminiscence therapy,

validation therapy, supportive psychotherapy, sensory
integration, also called snoezelen, and simulated presence
therapy. A Cochrane review has found no evidence that this is
effective. Reminiscence therapy (RT) involves the discussion of
past experiences individually or in group, many times with the
aid of photographs, household items, music and sound
recordings, or other familiar items from the past. A 2018 review
of the effectiveness of RT found that effects were inconsistent,
small in size and of doubtful clinical significance, and varied by
setting. Simulated presence therapy (SPT) is based on
attachment theories and involves playing a recording with
voices of the closest relatives of the person with Alzheimer's
disease. There is partial evidence indicating that SPT may
reduce challenging behaviors.

The aim of cognition-oriented treatments, which include reality

orientation and cognitive retraining, is the reduction of
cognitive deficits. Reality orientation consists of the
presentation of information about time, place, or person to
ease the understanding of the person about its surroundings
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and his or her place in them. On the other hand, cognitive
retraining tries to improve impaired capacities by exercising
mental abilities. Both have shown some efficacy improving
cognitive capacities.

Stimulation-oriented treatments include art, music and pet

therapies, exercise, and any other kind of recreational activities.
Stimulation has modest support for improving behavior, mood,
and, to a lesser extent, function. Nevertheless, as important as
these effects are, the main support for the use of stimulation
therapies is the change in the person's routine.

8.History
The ancient Greek and Roman philosophers and physicians
associated old age with increasing dementia. It was not until
1901 that German psychiatrist Alois Alzheimer identified the
first case of what became known as Alzheimer's disease, named
after him, in a fifty-year-old woman he called Auguste D. He
followed her case until she died in 1906 when he first reported
publicly on it. During the next five years, eleven similar cases
were reported in the medical literature, some of them already
using the term Alzheimer's disease. The disease was first
described as a distinctive disease by Emil Kraepelin after
suppressing some of the clinical (delusions and hallucinations)
and pathological features (arteriosclerotic changes) contained
in the original report of Auguste D. He included Alzheimer's
28
disease, also named presenile dementia by Kraepelin, as a
subtype of senile dementia in the eighth edition of his Textbook
of Psychiatry, published on 15 July, 1910.

For most of the 20th century, the diagnosis of Alzheimer's

disease was reserved for individuals between the ages of 45
and 65 who developed symptoms of dementia. The
terminology changed after 1977 when a conference on
Alzheimer's disease concluded that the clinical and pathological
manifestations of presenile and senile dementia were almost
identical, although the authors also added that this did not rule
out the possibility that they had different causes. This
eventually led to the diagnosis of Alzheimer's disease
independent of age. The term senile dementia of the Alzheimer
type (SDAT) was used for a time to describe the condition in
those over 65, with classical Alzheimer's disease being used to
describe those who were younger. Eventually, the term
Alzheimer's disease was formally adopted in medical
nomenclature to describe individuals of all ages with a
characteristic common symptom pattern, disease course, and
neuropathology.

The National Institute of Neurological and Communicative

Disorders and Stroke (NINCDS) and the Alzheimer's Disease and
Related Disorders Association (ADRDA, now known as the
Alzheimer's Association) established the most commonly used
29
NINCDS-ADRDA Alzheimer's Criteria for diagnosis in 1984,
extensively updated in 2007. criteria require that the presence
of cognitive impairment, and a suspected dementia syndrome,
be confirmed by neuropsychological testing for a clinical
diagnosis of possible or probable Alzheimer's disease. A
histopathologic confirmation including a microscopic
examination of brain tissue is required for a definitive
diagnosis. Good statistical reliability and validity have been
shown between the diagnostic criteria and definitive
histopathological confirmation.

30
 Bibliography
The websites that I referred for the completion of my project
are:
1. en.wikipedia.org
2. www.alz.org

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