ALZHEIMER’S DISEASE

AND IT’S
TREATMENT
 INTRODUCTION
 Alzheimer's disease (AD), also known as
Senile Dementia of the Alzheimer Type
(SDAT) or simply Alzheimer’s is the most
common form of dementia. This incurable,
degenerative, terminal disease was first
described by a German psychiatrist and
neuropathologist Alois Alzheimer in 1906
and was named after him.
 DEFINITION
 Alzheimer's disease (AD) is a slowly
progressive disease of the brain in
which there is progressive decline in one
or more areas of cognition that is
characterized by impairment of
memory,disturbances in reasoning,
planning,
language,calculation,judgement,
STATISTICS OF ALZHEIMER’S DISEASE

 Generally, it is diagnosed in people over

65 years of age, although the less-
prevalent early onset of Alzheimer’s can
occur much earlier.
 In 2006, there were 26.6 million
sufferers worldwide.
 Alzheimer’s is predicted to affect 1 in 85
people globally by 2050.
 Females preponderate males in a ratio
of 2:1 or 2:3
ETIOLOGY AND RISK
FACTORS

 Increased age

 Genetic abnormalities on

chromosome 1,14,19,21

 Elevated homocysteine

 Family history
PRECIPITATING FACTORS
The disease may be precipitated
by minimal damage from
 Head injury
 Systemic illness
 Anesthesia
 Smoking,viral infection
 Chronic illnesses
 High blood cholesterol
 Exposure to environmental toxins
(aluminium)
PATHOPHYSIOLOGY
 Genetic influence of changes in
chromosome

 Formation of β-amyloid plaques which

are dense4 insoluble deposits of protein
and cellular materials outside and
around the brain

 Devt.of plaques in the hippocampus that

encodes memories
 Degeneration of nerve terminals both
dentrites and axonal

 Changing of the internal supporting

structures (microtubules) which serve as
a tract to guide nutrients to the end of
t5he axon and back

 The protein which supports the tubule is

changed chemically and becomes
tangles

 Degeneration of the tubules and the

CONT….
 Decreases acetylcholine

 Gross brain changes like thickening of

the leptomeninges, shrunken gyri,
widened sulci enlarged ventricles
hippocampal shrinkage and generalized
atropy

 Memory failure,personality changes and

problem in carrying out ADL
WARNING SIGNS OF
ALZHEIMERS DISEASE
 Memory loss
 Changes in mood or behavior
 Difficulty in performing familiar tasks
 Changes in personality
 Disorientation
 Problem with use of language
 Poor judgement
 Problem with abstract thinking
 Loss of initiative
STAGES OF ALZHEIMER’S DISEASE
CLINICAL
MANIFESTATIONS
1) Early Stage (preclinical stage)

 This is considered as a mild/early stage and the

duration period is 2-4 years.
 Frequent recent memory loss, particularly of recent
conversations and events.
 Repeated questions, some problems expressing and
understanding language.
 Writing and using objects become difficult and
depression and apathy can occur.
 Drastic personality changes may accompany
functional decline.
 Need reminders for daily activities and difficulties with
sequencing impact driving early in this stage.
Shrinkage of hippocampus
 CONTINUED…..
2) Second stage (Mild alzheimers disease)
 This is considered as a middle/moderate stage and the
duration is 2-10 years.
 Can no longer cover up problems.

 Pervasive and persistent memory loss impacts life across

settings.
 Rambling speech, unusual reasoning, confusion about
current events, time, and place, poor judgement,careless in
work habits and household chores
 Potential to become lost in familiar settings, sleep
disturbances, and mood or behavioral symptoms like
agitation, apathy, dysphoria accelerate.
 Nearly 80% of patients exhibit emotional and behavioral
problems which are aggravated by stress and change.
 Slowness, rigidity, tremors, and gait problems impact
mobility and coordination.
 Need structure, reminders, and assistance with activities of
daily living.
CONTINUED…..
3) Moderate stage (8-12)
 Increased memory loss and confusion.
 Impaired word finding, circumlocution
 Problems recognizing family and friends.
 Inability to learn new things.
 Difficulty carrying out tasks that involve
multiple steps (such as getting dressed).
 Problems coping with new situations.
 Delusions and paranoia.
 Impulsive behavior.
 Paraphasias, Echolalia
 Palilalia, apraxia,
 In moderate AD, damage occurs in
areas of the brain that control language,
reasoning, sensory processing, and
conscious thought
 CONTINUED

4) Last stage
 This is considered as the severe stage and the duration is

12-20 years
 Confused about past and present. Loss of recognition of

familiar people and places

 Generally incapacitated with severe to total loss of verbal

skills.
 Unable to care for self. Falls possible and immobility

likely.
 Problems with swallowing, incontinence, and illness.

 Extreme problems with mood, behavioral problems,

hallucinations, and delirium.

 Patients need total support and care, and often die from

infections or pneumonia
Plaques and tangles are widespread throughout the
brain
 Diagnosis of
Alzheimer’s

Disease
Alzheimer's disease is usually diagnosed
clinically from the patient history, collateral
history from relatives, and clinical
observations, based on the presence of
characteristic neurological and
neuropsychological features
 Advanced medical imaging with computed
tomography (CT) or magnetic resonance
imaging (MRI)
 single photon emission computer
tomography (SPECT) or positron
emission tomography
 (PET) can be used to help exclude other
cerebral pathology or subtypes of
dementia.
 The diagnosis can be confirmed with
very high accuracy post-mortem when
.

PET scan of the brain of a person with AD showing a loss

of function in the temporal lobe.
 Diagnostic

Tools
Neuropsychological tests such as the
mini-mental state examination (MMSE).
 Psychological tests
 Lab tests
(CBC,Urinalysis,ESR ,Electrolytes,TFT,LF
T,RFT,SrB12 levels,Calciun,syphilis,HIV)
 Treatment
 Although there is currently no way to cure
Alzheimer's disease or stop its progression,
Mild AD –Moderate AD
 1. Cholinesterase inhibitors increase
the levels of acetylcholine in the brain,
which plays a key role in memory and
learning. Cholinesterase inhibitors most
commonly prescribed for mild to moderate
Alzheimer's disease include Tacrine 5-
10mg Hs, Aricept (donezepil HCL 1.5 mg
Bd), Exelon (rivastigmine), and Razadyne
(galantamine) 4-12 mg Bd.
 Continued
Moderate/Severe AD:
Namenda (memantine) regulates
glutamate in the brain, which plays a key
role in processing information.
 Alpha tocopheral( vit E) and Seligiline can
be administered to combat the
progression
 Extract og Ginko biloba and
propentofylline improves the cognitive
function
 Memory enhancing drugs : Acetylcholine
precursors like choline,lecithin,and deanol
OTHER MEDICATIONS
 Antipsychotic drugs (Haloperidol,
Thioridazine)
 Citalopram , Sertraline can be used to
treat depression
 Sodium Valproate and Tegretol are

Used to treat severe aggression

NON PHARMACOLOGICAL
MEASURES
 Environmental manipulation
 Massage,Aroma therapy,music therapy
 Behavioral management
 Aerobic weight bearing exercises
 Food rich in Beta carotine,vit c,vit E and
vegetables
 Consume a low fat diet
 Care giver support
SUPPORTIVE CARE
 Adult day care
 Respite care
 Assisted living facilities
 Nursing homes
NURSING MANAGEMENT
 MSE
 Be polite and don’t be frustrated in pts
with aggressive behavior
 Use multiple sensory modalities to send
messages
 Continuously apply interventions to
enhance memory
 Provide orientation to the environment
 Meet the self care and emotional needs
NURSING DIAGNOSIS
 Impaired verbal communication related
to neuronal degeneration
 Disturbede thought process
 Self care deficit
 Urge urinary incontinence
New Treatments for
⦿ A.D
A molecule designed by a Purdue University researcher to
stop the debilitating symptoms of Alzheimer's disease has
been shown in its first phase of clinical trials to be safe and
to reduce biomarkers for the disease.
⦿ The molecule, called a beta-secretase inhibitor, prevents the
first step in a chain of events that leads to amyloid plaque
formation in the brain. This plaque formation creates fibrous
clumps of toxic proteins that are believed to cause the
devastating symptoms of Alzheimer's.
⦿ Researchers at Mount Sinai School of Medicine have found
that a compound called NIC5-15, might be a safe and
effective treatment to stabilize cognitive performance in
patients with mild to moderate Alzheimer's disease. The two
investigators, Giulio Maria Pasinetti, M.D., Ph.D. , and Hillel
Grossman, M.D., presented Phase IIA preliminary clinical
findings at the Alzheimer's Association 2009 International
Conference on Alzheimer's Disease (ICAD) in Vienna on July
12.
 Continued
 NIC5-15's potential to preserve
cognitive performance will be further
evaluated in a Phase IIB clinical trial.
Early evidence suggests that NIC5-15 is
a safe and tolerable natural compound
that may reduce the progression of
Alzheimer's disease-related dementia by
preventing the formation of beta-
amyloid plaque, a waxy substance that
accumulates between brain cells and
impacts cognitive function.
 Questions
 What are the three stages of
Alzheimer’s Disease?
 What are some of the diagnostic tools of
diagnosing Alzheimer’s Disease?
 What drugs are used to treat
mild/moderate Alzheimer’s Disease?
 Which drug is most commonly used to
treat Alzheimer’s Disease?
 Have current pharmaceutical agents
been successful in slowing the progress
of Alzheimer’s Disease?
 Why is it important to develop
‘biomarkers’ for Alzheimer’s Disease?