By

M. MeenakshiSivapriya
XII B3
School: Shrishti Vidyashram
Year: 2014-2015



What are we going to learn?

Acknowledgement
What is Alzheimers disease?
Stages of Alzheimers disease
Causes of Alzheimers disease
How is Alzheimers disease diagnosed?
Alzheimers vs. Parkinsons disease
Preventive measures
Treatments and cures
Some interesting facts
Conclusion
Bibliography














Acknowledgement

Firstly, I would like to thank my parents for encouraging and enabling me to
collect facts for this project. Also, I thank the almighty for giving me
interest and joy in completing this work.

I also express my heart felt gratitude to my biology teachers Mrs. Anuradha
and Mrs. Susan Philip for giving me this wonderful opportunity and guiding
me throughout.

I sincerely thank our assistant teacher Mrs. Vijayakumari for her valuable
suggestions and constant encouragement.













What is Alzheimer s Disease?

Alzheimers disease (AD), also known in medical literature as Alzheimer
disease, is the most common form of dementia. There is no cure for the
disease, which worsens as it progresses, and eventually leads to death. It
was first described by German psychiatrist and neuropathologist Alois
Alzheimer in 1906 and was named after him. Most often, AD is diagnosed in
people over 65 years of age, although the less-prevalent early-onset
Alzheimers can occur much earlier. In 2006, there were 26.6 million people
worldwide with AD. Alzheimers is predicted to affect 1 in 85 people globally
by 2050.
Although Alzheimers disease develops differently for every individual, there
are many common symptoms. Early symptoms are often mistakenly
thought to be 'age-related' concerns, or manifestations of stress.In the
early stages, the most common symptom is difficulty in remembering
recent events, known as short term memory loss.
When AD is suspected, the diagnosis is usually confirmed with tests that
evaluate behavior and thinking abilities, often followed by a brain scan if
available. However, examination of brain tissue is required for a definitive
diagnosis. As the disease advances, symptoms can include confusion,
irritability, aggression, mood swings, trouble with language, and long-term
memory loss. As the person's condition declines they often withdraw from
family and society. Gradually, bodily functions are lost, ultimately leading to
death.

Since the disease is different for each individual, predicting how it will
affect the person is difficult. AD develops for an unknown and variable
amount of time before becoming fully apparent, and it can progress
undiagnosed for years. On average, the life expectancy following diagnosis
is approximately seven years. Fewer than 3% of individuals live more than
14 years after diagnosis.

Current treatments only help with the symptoms of the disease. There are
no available treatments that stop or reverse the progression of the disease.
Mental stimulation, exercise, and a balanced diet have been suggested as
ways to delay cognitive symptoms in healthy older individuals, but there is
no conclusive evidence supporting an effect. Thus, AD is one of the most
costly diseases to society.


Stages of Alzheimers Disease
We must not confuse aging effects with Alzheimers disease. The
following stages of AD will help us understand the differences.
Effects due to aging:
Forgetting things occasionally.
Misplacing items sometimes.
Minor short-term memory loss.
Forgetting that memory lapses happened.

Early stage Alzheimers:
Absent-mindedness.
Forgetting appointments.
Slight changes seen by close loved ones.
Some confusion in situations outside the familiar.

Middle stage Alzheimers:
Deeper difficulty remembering recently learned information.
Deepening confusion in many circumstances.
Speech impairment.
Repeatedly initiating the same conversation.

Late stage Alzheimers
More aggressive or passive.
Some loss of self-awareness.
Debilitating cognitive deficit.
More abusive, anxious, or paranoid.



CAUSES OF ALZHEIMERS


The cause for most Alzheimers cases is still mostly unknown except for 1%
to 5% of cases where genetic differences have been identified. Several
competing hypotheses exist trying to explain the cause of the disease.

Genetics
Around 0.1% of the cases are familial forms
of autosomal dominant inheritance, which usually have an onset before age
65. This form of the disease is known as early onset familial Alzheimers
disease. Most of autosomal dominant familial AD can be attributed to
mutations in one of three genes: those encoding amyloid precursor
protein (APP) and presenilins 1 and 2. Most mutations in the APP and
presenilin genes increase the production of a small protein called A

42,
which is the main component of Senile plaques. Some of the mutations
merely alter the ratio between A42 and the other major forms without
increasing A42 levels.

CHOLINERGIC HYPOTHESIS
The oldest, on which most currently available drug therapies are based, is
the cholinergic hypothesis, which proposes that AD is caused by reduced
synthesis of the neurotransmitter acetylcholine. The cholinergic hypothesis
has not maintained widespread support, largely because medications
intended to treat acetylcholine deficiency have not been very effective.
Other cholinergic effects have also been proposed, for example, initiation of
large-scale aggregation of amyloid, leading to
generalized neuroinflammation.

Also, there is tentative evidence that exposure to air pollution may be a
contributing factor to the development of Alzheimers disease.





How is AD diagnosed?

Alzheimers disease is usually diagnosed based on the person's history, and
observations of the person's behaviors.
The presence of characteristic neurological and neuropsychological features
and the absence of alternative conditions is supportive. 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 Alzheimers disease.

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. The diagnosis can be confirmed with very high
accuracy post-mortem when brain material is available and can be
examinedhistologically.

The criteria requires that the presence of cognitive impairment, and a
suspected dementia syndrome, be confirmed by neuropsychological
testing for a clinical diagnosis of possible or probable AD.
A histopathologic confirmation including a microscopic examination of brain
tissue is required for a definitive diagnosis. Eight cognitive domains are
most commonly impaired in ADmemory, language, perceptual
skills, attention, constructive abilities, orientation, problem solving and
functional abilities.

EARLY DIAGNOSIS
Emphasis in Alzheimers research has been placed on diagnosing the
condition before symptoms begin. A number of biochemical tests have been
developed to allow for early detection. One such test involves the analysis
of cerebrospinal fluid for beta-amyloid or tau proteins. Searching for these
proteins using a spinal tap can predict the onset of Alzheimers with
a sensitivity of between 94% and 100%. When used in conjunction with
existing neuroimaging techniques, doctors can identify people with
significant memory loss who are already developing the disease.
Alzheimers vs. Parkinsons disease

Similarities:
The two diseases are not related but they do share some similarities. Both
Alzheimers and Parkinsons disease have a late onset in life, usually after
the age of 50. Both diseases are neurodegenerative, meaning that brain
cells (neurons) become damaged and die during the course of the disease.
They are also both progressive, so they get worse over time.
In the late stages of both diseases, the neurodegeneration can ultimately
lead to dementia a severe impairment in memory, judgment, orientation,
and executive functioning. Approximately two out of every three dementia
cases are caused by Alzheimers disease, making it by far the most common
cause. Meanwhile, dementia due to Parkinsons accounts for a much smaller
portion of all dementia cases.
Differences:
Parkinsons disease is primarily a movement disorder that can eventually
result in memory problems and dementia in about 50% of patients. Many
individuals with Parkinsons may never have memory problems during the
course of their illness.
Parkinsons disease results from the loss of dopamine-producing neurons in
an area of the brain called the substantia nigra. Dopamine is needed in that
part of the brain to control movement and coordination, and it is estimated
that it takes a 60-80% loss of these dopaminergic neurons before
symptoms become outwardly apparent. These symptoms include a resting
tremor (shaking at rest), muscle rigidity, slowed movements, and impaired
coordination. Over time, as the disease progresses, the benefits of the
drugs often diminish or become less consistent.
Now with Alzheimers disease, the initially affected brain areas are the
hippocampus and the entorhinal cortex, which are critical for learning and
memory. Therefore it follows that the early symptoms of Alzheimers are
cognitive in nature. In Alzheimers it is the neurotransmitter acetylcholine
that is progressively diminished over the course of the disease. This
worsening of memory and general intellect can progress and become severe
without any effect on the patients coordination or movement ability.
Preventive Measures

At present, there is no definitive evidence to support that any particular
measure is effective in preventing AD. Global studies of measures to
prevent or delay the onset of AD have often produced inconsistent results.
Epidemiological studies have proposed relationships between certain
modifiable factors, such as diet, cardiovascular risk, pharmaceutical
products, or intellectual activities among others, and a population's
likelihood of developing AD. Only further research, including clinical trials,
will reveal whether these factors can help to prevent AD.

MEDICATION

Although cardiovascular risk factors, such
as hypercholesterolaemia, hypertension, diabetes, and smoking, are
associated with a higher risk of onset and course of AD, statins, which
are cholesterol lowering drugs, have not been effective in preventing or
improving the course of the disease.

Long-term usage of non-steroidal anti-inflammatory drugs (NSAIDs) is
associated with a reduced likelihood of developing
AD. Human postmortem studies, in animal models, or in vitro investigations
also support the notion that NSAIDs can reduce inflammation related to
amyloid plaques. However, trials investigating their use as palliative
treatment have failed to show positive results, apparently because the brain
NSAID concentration after an oral NSAID dose is exceedingly small.

No prevention trial has been completed. Hormone replacement therapy,
although previously used, may increase the risk of dementia.








LIFESTYLE

People who engage in intellectual activities such as reading, playing board
games, completing crossword puzzles, playing musical instruments or
regular social interaction show a reduced risk for Alzheimers disease. 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 AD syndrome, but is not
related to earlier death after diagnosis. Learning a second language even
later in life seems to delay getting Alzheimer disease. Physical activity is
also associated with a reduced risk of AD.

DIET

People who eat a Mediterranean diet have a lower risk of AD, and it may
improve outcomes in those with the disease. Those who eat a diet high in
saturated fats and simple carbohydrates have a higher risk. The
Mediterranean diet's beneficial cardiovascular effect has been proposed as
the mechanism of action. There is limited evidence that light to moderate
use of alcohol, particularly red wine, is associated with lower risk of
AD. There is tentative evidence that caffeine may be protective. A number
of foods high in flavonoids such as cocoa, red wine, and tea may decrease
the risk of AD.










Treatments & Cures
Five medications are currently used to treat the cognitive problems of AD:
Acetylcholinesteraseinhibitors (tacrine, rivastigmine, galantamine
and donepezil) and the other is an NMDA receptor antagonist. The benefit
from their use is small. No medication has been clearly shown to delay or
halt the progression of the disease.

Reduction in the activity of the cholinergic neurons is a well-known feature
of Alzheimers 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 Alzheimers disease and
some evidence for their use in the advanced stage.

Only donepezil is approved for treatment of advanced AD dementia. The
use of these drugs in mild cognitive impairment has not shown any effect in
a delay of the onset of AD.

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 and are mild to moderate in severity. Less common secondary
effects include muscle cramps, decreased heart rate (bradycardia),
decreased appetite and weight, and increased gastric acid production.












Glutamate is a useful 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 Alzheimers 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 be moderately efficacious in the treatment of moderate to
severe Alzheimers disease. Its effects in the initial stages of AD are
unknown.

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".


Antipsychotic drugs are modestly useful in
reducing aggression and psychosis in Alzheimers disease with behavioral
problems, but are associated with serious adverse effects, such
as stroke, movement difficulties or cognitive decline, that do not permit
their routine use. When used in the long-term, they have been shown to
associate with increased mortality.

Huperzine A, while promising requires further evidence before it use can be
recommended.






Some interesting facts

Nearly half of adults aged 85 and over have Alzheimers disease.
Out of approximately 5.4 million Americans with Alzheimers, more than
half may not know they have it.
More women than men have Alzheimers disease.
Early-onset Alzheimers can develop in people as young as age 30.
In America, a new case of Alzheimers develops every 68 seconds; by
2050, the incidence will increase to every 33 seconds.
Alzheimers is the 6th-leading cause of death in the U.S., and the 5th-
leading cause of death in adults aged 65 and over.
Over 15 million Americans are unpaid caregivers for someone with
Alzheimers disease or another form of dementia.
In 2012, the average annual cost of health care and ltc services for
someone with Alzheimers was $43,847.
An estimated 800,000 Americans with Alzheimers are living alone.













Conclusion

So to conclude Alzheimers is a disease that remains a mystery with the
cause and the cure yet to be found. Though Alzheimers cant be cured or
reversed at present much can be done to help the patient and their family
live through the course of the illness with less discomfort and more dignity.

From our part, just as we exercise and keep our body healthy and fit, we
must take up brain games like crosswords or chess to keep our brains
fresh. There are proven results that confirm this. Cures are being
investigated and hopefully one day this disease will be cured and if not
better understood.


















Bibliography

Cohen. E (1999) ALZHEIMERS DISEASE McGraw-Hill Professional
publishing

Strock. M (1996) ALZHEIMERS DISEASE, DIAGNOSIS, CURE AND
TREATMENT DIANE Publishing

ALZHEIMERS DISEASE 2007 [online]
(http://www.Alzheimers.org.uk/

ALZHEIMERS DISEASE INTERNATIONAL 2007 [online]
http://www.alz.co.uk/Alzheimers/

http://www.cartoonstock.com/lowres/jdo0864l.jpg

http://www.colorado.edu/kines/Class/IPHY3730/image/figure4-9.jpg

http://en.wikipedia.org/wiki/Alzheimers_disease