Penyebab yang pasti belum diketahui. Beberapa alternatif penyebabyang telah dihipotesa adalah 1 intoksikasi logam, 2 gangguan fungsi imunitas, 3 infeksi virus, 4 polusi udara/industri, 5 trauma, 6 neurotransmiter, 7 defisit formasi sel-sel filament, 8 presdiposisi heriditer. 9 Dasar kelainan patologi penyakit alzheimer terdiridari degenerasi neuronal, kematian daerah spesifik jaringan otak yangmengakibatkan gangguan fungsi kognitif dengan penurunan daya ingat secaraprogresif.10 Adanya defisiensi faktor pertumbuhan atau asam amino dapatberperan dalam kematian selektif neuron. Kemungkinan sel-sel tersebutmengalami degenerasi yang diakibatkan oleh adanya peningkatan calsiumintraseluler, kegagalan metabolisme energi, adanya formasi radikal bebas atauterdapatnya produksi protein abnormal yang non spesifik.11Penyakit alzheimer adalah penyakit genetika, tetapi beberapapenelitian telah membuktikan bahwa peran faktor genetika, tetapi beberapapenelitian telah membuktikan bahwa peran faktor non-genetika (lingkungan)juga ikut terlibat, dimana faktor lingkungan hanya sebagai pencetus faktorgenetika.

1. Faktor genetik2. Faktor infeksi

Ada hipotesa menunjukkan penyebab infeksi virus pada keluarga penderita alzheimer yang dilakukan secara immuno blot analisis, ternyata diketemukan adanya antibodi reaktif. Infeksi virus tersebut menyebabkan infeksi pada susunan saraf pusat yang bersipat lambat, kronik dan remisi. Beberapa penyakit infeksi seperti Creutzfeldt-Jacob disease dan kuru, diduga berhubungan dengan penyakit alzheimer.

3. Faktor lingkunganEkmann (1988), mengatakan bahwa faktor lingkungan juga dapat berperan dalam patogenesa penyakit alzheimer. Faktor lingkungan antaralain, aluminium, silicon, mercury, zinc. Aluminium merupakan neurotoksik potensial pada susunan saraf pusat yang ditemukan neurofibrillary tangles (NFT) dan senile plaque (SPINALIS). Hal tersebut diatas belum dapat dijelaskan secara pasti, apakah keberadaan aluminum adalah penyebab degenerasi neurosal primer atau sesuatu hal yang tumpang tindih. Pada penderita alzheimer, juga ditemukan keadan ketidak seimbangan merkuri, nitrogen, fosfor, sodium, dengan patogenesa yang belum jelas.

4.Faktor imunologisBehan dan Felman (1970) melaporkan 60% pasien yang menderita alzheimer didapatkan kelainan serum protein seperti penurunan albumin dan peningkatan alpha protein, anti trypsin alphamarcoglobuli dan haptoglobuli. Heyman (1984), melaporkan terdapat hubungan bermakna dan meningkat dari penderita alzheimer dengan penderita tiroid. Tiroid Hashimoto merupakan penyakit inflamasi kronik yang sering didapatkan pada wanita muda karena peranan faktor immunitas.

5. Faktor traumaBeberapa penelitian menunjukkan adanya hubungan penyakit alzheimer dengan trauma kepala. Hal ini dihubungkan dengan petinju yang menderita demensia pugilistik, dimana pada otopsinya ditemukan banyak neurofibrillary tangles.

6. Faktor neurotransmiter

Alzheimer's disease is a chronic, progressive, and is a degenerative disorder of the brain and are

known to affect memory, cognition and ability to care for themselves.

(Suddart, & Brunner, 2002).

Alzheimer's is a degenerative disease characterized by memory loss, intellectual, and

personality. Not curable, treatment is aimed at stopping the progression of disease and

improving patient independence.

(Dr. Sofi Kumala Dewi, et al, 2008)

Alzheimer's is a devastating disease and cause paralysis, which occurs mainly in people aged 65

years and older (patofiologi: clinical concepts of disease processes, is also a disease with

degenerative disorders of the brain cells and causes disruption of intellectual functioning, these

diseases occur in men and women and according to documents occur at a specific person at the

age of 40 years.

(Medical Surgical Nursing: Volume 1 p. 1003)

So that Alzheimer's is a chronic disease, degenerative characterized by memory loss,

intellectual, personality which can result in reduced ability to care for themselves. The disease

attacks people aged 65 years and older.

2.1.1 Alzheimer's Dementia

Diagnosis is made according to the completeness of clinical information, pathology and

similarities syndrome

of dementia. Diagnosis of Alzheimer's divided into a definite diagnosis, probable and possible.1

2.2 Classification

Dementia can be divided into reversible and irreversible dementia that is: 1.2

reversible:

- Alcoholism

- Disturbance pasikiatri

- Normal Pressure Hydrocephalus

- Vascular Dementia

irreversible:

Alzheimer-Dementia

-Pick's Disease

-Parkinson 's Disease Dementia

2.3 Etiology

Alzheimer's disease is a common type of dementia of unknown cause.

Autopsy studies reveal that more than half the patients who died

because of dementia Alzheimer type senil experiencing this disease.

2.4 Pathophysiology

Some of the theories underlying the pathophysiology of Alzheimer's dementia include: 1,3,4

1. Neurotransmitter abnormalities. Neurotransmitter abnormalities that were most responsible

pathophysiologic are acetylcholine and norepinephrine, both hypothesized to be

hipoaktif in diseases with cytoskeletal elements, especially protein berfosforilasi,

although other cytoskeletal proteins were also found. Creasing neurofibriler is

not unique to Alzheimer's disease, because the situation is also found in

Down syndrome, dementia pugilistic (punch-drunk syndrome) dementia complex

Parkinson from Guam, Hallervorden-Spatz disease, and brain and the elderly

to normal. Neurofibriler clutter usually found in the cortex, hippocampus, substantia

nigra, and locus sereleus.

2. Amyloid precursor protein. The gene for amyloid precursor protein is in the arm

length of chromosome 21. Through the process of differential splicing, in fact there

four forms of amyloid precursor protein. Beta/A4 protein, which is the content

of the senile plaques, is a peptide with 42 amino acids which are

destruction of the amyloid precursor protein products. In Down syndrome (trisomy 21),

There are three prints of amyloid precursor protein, and in diseases where the mutations occur

at codon 717 in the amyloid precursor protein gene, a pathological process

result in excessive deposition of protein beta/A4. The question of whether the process on

abnormal amyloid precursor protein is an important primary cause of the

Alzheimer's disease remain unanswered. However, many research groups are actively

studying the normal metabolic process of the amyloid precursor protein and the process on

patients with Alzheimer type dementia in an attempt to answer the question

them. Senile plaques are also known as amyloid plaques, is far more indicative for

Alzheimer's disease, although the situation is also found in Down syndrome

and to some extent, in normal aging.

3. Other potential causes. Other causative theories have been proposed to explain

the development of Alzheimer's disease. One theory is that the abnormalities in the regulation

membrane phospholipid metabolism causing a shortage of liquid membrane is

more rigid than normal. Some researchers have used imaging

molecular resonance spectroscopic (molecular resonance spectroscopic: MRS) to examine the

hypothesis that in patients with Alzheimer type dementia. Toxicity

Aluminium has also been hypothesized as a causative factor, because the levels of aluminum

high have been found in the brains of some patients with Alzheimer's disease.

A gene (E4) have been associated in the etiology of Alzheimer's disease. People with a

copy of the gene suffer from Alzheimer's disease three times more often than people without

the gene

E4. People with two E4 gene had eight times as likely to suffer from the disease

more often than those without E4 gene.

2.5 Clinical Manifestation

Clinical manifestations in patients with demesia include: 2,4,5

1. Amnesia / memory, especially short-term memory. In normal parents, he

can not remember the name of his neighbor, but he knew this man was his neighbor. In

patients

Alzheimer's, he not only forgot the name of his neighbors but also forget that the person is

its neighbors.

2. Difficulty doing the usual routine activities, such as do not know how to unlock

clothes or do not know the sequences of preparing food.

3. Difficulty speaking. Generally in the elderly find it difficult to get the word

the right, but people with Alzheimer's will forget simple words or substitute

a word with the word unusual.

4. Disorientation of time and place. We sometimes forget where we will go or what day

this, but people with Alzheimer's may get lost in places that are familiar to him, forgetting the

where he is today, do not know how he arrived at this place, including whether the current

This night or day.

5. The decrease in deciding something or executive functions, for example can not be

decided to use warm clothes for cold weather or otherwise.

6. One place the goods. A person can temporarily misplaced wallet

or keys. People with Alzheimer's may put things in unusual places, such as

watch on the box of sugar.

7. Changes in behavior. One can be happy or sad from time to time.

People with Alzheimer's can change the mood or emotion is not unusual for no reason that can

be

be accepted.

8. Changes in People with Alzheimer's behavior will look different than usual, it will be

suspicious, irritable, depressed, apathetic or easy rampage, especially when the problem

memory difficulties caused him to do something.

9. Loss of initiative. Sitting in front of the TV for hours, sleeping more than usual or not

show interest in this hobby for ditekuninya.

The characteristics of dementia in Alzheimer's

1. Predementia:

· Mild cognitive disorder (8 years before diagnosis)

· Memory Deficit

· Apathy

2. Early onset dementia

· Improved memory & learning disorders

· Disorders of language, vocabulary & word ↓, ↓ oral and written language skills

· Disturbance of perception (agnosia)

· Impaired movements (apraxia)

· Visible stupid

· Lack of initiation to perform activities

3. Dementia MODERA

· Progressive deterioration

· Not being able to read & write

· Impaired long-term memory

· Substitution use of the word (parafasia)

· Misidentification

· Labile

· Easily angry

· Delusions

· Incontinence urinary system

4. Dementia stage (advanced)

Unable to take care of themselves

· Loss of total verbal ability

· Aggressive

· Apathy extreme

· Deterioration of muscle mass & mobility

· Loss of ability to eat

Based on the stage:

Stage I (1-3 years old diseases)

· Memory: The new memory defects (Leaning), mild impairment of recall

· Visuospatial abilities: topographical disorientation, not able to form complex

· Language: difficult to form a new word, anomia

· Personality: indifference, sometimes irritable

· Psychiatric manifestations: sadness or some delusional

· Motor system: normal

· EEG: normal

· CT / MRI: normal

· PET / SPECT: bilateral posterior hypometabolism / hyperfusion

Stage II (3-10 years old diseases)

· Memory: The new memory (Leaning) & severe impairment of recall

· Visuospatial abilities: spatial disorientation, poor contructions

Languages: fluent

· Aphasia calculation: akalkulation

· Personality: Indifference & irritability

· Manifestation of psychiatry: delusions

· Motor system: restlessness, pacing

· EEG: slow background rhythm

· CT / MRI: normal or ventricular and sulcal enlargement

· PET / SPECT: bilateral parietal and frontal hypometabolism / hyperfusion

Stage III (disease 8-12 years old)

· Intellectual function: severely deteriorated

· Motor system: limb rigidity and flexion poeture

· Sphincter control: urinary and fecal

· EEG: diffusely slow

· CT / MRI: ventricular and sulcal enlargement

· PET / SPECT: bilateral parietal and frontal hypometabolism / hyperfusion

2.6 History and Physical Examination 1.6

A. The medical history includes:

1. General medical history: an interview covering medical disorder that can cause

dementia such as coronary heart disease, heart valve disorders, heart disease collagen,

hypertension, hyperlipidemia, diabetes, peripheral arteriosclerosis, hypothyroidism.,

neoplasms,

infeksikronik (syphilis, AIDS)

2. General Neurology History: Interview neurological history as a history of stroke, TIA,

trauma capitis, central nervous system infections, a history of epilepsy and brain surgery

because of tumor or

hydrocephalus. Accompanying symptoms of dementia such as sensory motor disorders,

impaired

running, coordination and balance disturbances are suddenly in the early phase indicates

focal neurologic deficits that lead to vascular dementia

3. Neurobehaviour History: Information from a family of penurunanfuingsi cognition,

intellectual ability dalama daily activities danperubahan behavior is very

important in the diagnosis of dementia.

4. Psychiatric History: History is important to determine whether psychiatric patients

experiencing depression, psychosis, personality changes, aggressive behavior, delusions,

hallucinations,

paranoid thoughts, and whether this interference occurs before or after the onset of dementia.

5. A history of poisoning, nutrition, drugs: Toxicity of heavy metals, pesticides, glues and

fertilizer, nutritional deficiencies, chronic alcohol consumption can lead to dementia, although

not specific to VAD. The use of antidepressants, anticholinergics and herbs

can disrupt the function of cognition.

6. Family history: The examiner must explore all of the incidence of dementia in the family.

B. Objective examination include:

1. A general physical examination: Includes observation of appearance, the sign-tandavital,

arteriosclerosis,

vascular risk factors.

2. Neurological examination: Impaired walking, impaired strength, tone or motor control,

sensory disturbances and visual field of brain nerve disorders, impaired balance and

reflex disturbances.

3. Mental status examination: Mental status examination meliputimemori cognition,

orientation,

language, cortical function, is associated with math, writing, praxis, gnosis, visuospasial and

visuopersepsi.

4. Examination of the functional activity: An examination of the patient performanyata

activities of daily life during this atausaat premorbid.

5. Psychiatric examination: This examination is to determine the physically kondisimental

dementia, whether he suffered from mental depression, delirium, anxiety, or experiencing

symptoms

psychotic.

2.6 Examination of Alzheimer's Dementia

To determine this disease can do some investigation, namely: 6,8,10

A. Neuropathology

Definitive diagnosis can not be enforced without the confirmation of neuropathology. In general

found atrophy of the bilateral, symmetrical, often the brain weight was 1000 g (850 -

1250gr).

Some studies reveal atrophy more prominent in temporoparietal lobes, anterior

frontal, whereas the occipital cortex, primary motor cortex, somatosensory system remains

intact

(Jerins 1937). Abnormalities in Alzheimer's disease neuropathology consists of:

a. Neurofibrillary tangles (NFT)

Neuronal cytoplasm is made of abnormal filaments containing the proteins

neurofilament, ubiquine, epitoque. NFT are also found in the neocortex, hippocampus,

amygdala,

substantia alba, locus ceruleus, dorsal raphe nucleus of the brain stem. NFT than obtained in

Alzheimer's disease, also found in the brains of elderly, Down syndrome, Parkinson's, SSPE,

ektrapiramidal syndrome, supranuklear palsy. NFT density correlated with the severity

of dementia.

b. Senile plaque (SP)

Is a complex structure that occurs due to degeneration of nerve endings containing

filamenfilamen

abnormal, ektraseluler amyloid fibers, astrocytes, microglia. Amloid precursor protein

contained in the SP is associated with chromosome 21. Senile plaque is mainly contained

the neocortex, amygdala, hippocampus, cortex piriformis, and little was found in the cortex

primary motor, somatosensory cortex, visual cortex, and auditory. Senile plaque is also

present in peripheral tissues.

Perry (1987) said that the density of senile plaques associated with decreased cholinergic.

The second picture of histopathology (NFT and senile plaque) are characteristic features for

Alzheimer's disease patients.

c. Degeneration of neurons

On microscopic examination of change and death of neurons in Alzheimer's disease is very

selectively. Death of neurons in the neocortex mainly found in pyramidal neurons lobe

temporal and frontal. Also found in the hippocampus, amygdala, brain stem nuclei

including the locus serulues, raphe nucleus and substanasia nigra.

Cholinergic neuronal cell death mainly in the nucleus basalis of meynert, and cell

especially the noradrenergic locus ceruleus and raphe nuclei of cells in the dorsal serotogenik,

nucleus of the dorsal tegmentum. It has been found of nerve growth factor on cholinergic

neurons

which degenerates on the lesions of experimental animals and it is an expectation in

treatment of Alzheimer's disease.

d. Changes vakuoler

It is an oval shaped neuronal cytoplasm and nucleus can shift.

The amount of this vakuoler significantly associated with the number of NFT and SP, this change

often obtained at temporomedial cortex, amygdala and insula. Was never found

in the frontal cortex, parietal, occipital, hippocampus, cerebellum and brain stem.

e. Lewy body

Intraneuronal cytoplasmic part that is widely available on enterhinal, gyrus

cingulate cortex, insula, and amygdala. A small number in the frontal cortex, temporal,

parietal, occipital. Cortical Lewy body is the same as immunoreaktivitas that occur in the brain

stem Lewy body in Parkinson's disease histopathology images. Hansen et al

states Lewy body variant of Alzheimer's disease is.

2. Examination NeuropsikologikAlways cause symptoms of Alzheimer's disease dementia. The function checks neuropsikologikis to determine the presence or absence of general cognitive dysfunction and find outin detail the pattern of deficit. Psychological test also aims to assess the function of theshown by some sections of different brain such as memory impairment, loss ofexpression, calculation, attention and understanding language. Neuropsychological evaluationSystematic has important diagnostic function because:1. The existence of cognitive deficits associated with early dementia that can be known whenminor changes that occur due to normal aging.2. Neuropsikologik comprehensive examination allows to distinguishglobal cognitive disorders in dementia with selective deficits caused byFocal dysfunction, metabolic factors, and psychiatric disorders3. Identify picture neuropsikologik abnormalities caused by dementia

due to various causes. The Consortium to Establish a Registry for Alzheimer's Disease(CERALD) present a neuropsychological assessment procedures withbatrey use tool that manifests impaired cognitive function, whichexamination consists of:· Verbal Fluency animal category· Modified Boston naming test· Mini-mental state· Word list memory· Constructional praxis· Word list recall· Word list recognitionThis test takes 30-40 minutes and <20-30 minutes in control.3. CT Scan and MRIIs a non-invasive method of high resolution to see the quantification of changesvolume of brain tissue in Alzheimer's patients antemortem. These checks are instrumental in getting rid of the possible causes of dementia other than Alzheimer's asmultiinfark and cerebral tumors. Overall cortical atrophy and ventricular enlargement are bothis the dominant image of a highly specific marker in this disease. But the pictureIt is also found in other dementias such as multiinfark, Parkinson's disease, Binswanger soit is hard to distinguish from Alzheimer's disease.Thinning of the cerebral substantia alba and ventricular enlargement correlated with the severity of symptomsclinics and mini-mental status examination. On MRI found an increase in intensityin cortical regions and periventrikuler (Capping the anterior horn in the lateral ventricles). CappingThis is a predilection for early dementia. In addition to abnormalities found in cortical, pictureatrophy was also seen in subcortical areas such as the atrophy of the hippocampus, amygdala, andsisterna basal enlargement and fissures sylvii.Seab et all, states are more sensitive MRI to distinguish dementia from Alzheimer's diseasewith other causes, taking into account the size (atrophy) of the hippocampus.4. EEGUseful to identify activities that suklinis resurrection. Being on the diseaseAlzheimer changes in slow-wave obtained in a non-specific frontal lobe5. PET (Positron Emission Tomography)In people with Alzheimer's, PET results found decreased blood flow, O2 metabolism, andcerebral glucose area. Up take I.123 greatly decreased in the parietal region, these results are verycorrelated with cognitive dysfunction and always and in accordance with observationsneuropathology studies.6. SPECT (Single Photon Emission Computed Tomography)Activity I. 123 ratio was lowest in patients with Alzheimer's parieral. These abnormalities correlated withextent of damage and functional deficits kogitif. Both of these checks (SPECT and PET) are notused routinely.7. Laboratory bloodNo specific laboratory tests in patients with Alzheimer's. Examination

this laboratory only to rule out other causes of dementia such asroutine blood tests, B12, calcium, phosphorous bombs, BSE, renal and hepatic function, thyroid, folic acid,syphilis serology, skreening antibody selectively performed.2.7Kriteria Diagnosis

Diagnostics criteria for dementia in Alzheimer's disease emphasize the presence of interference

memory and with the presence of at least one other symptom of cognitive impairment

(Aphasia, apraxia, agnosia, or executive function is abnormal). Criteria for diagnosis as well

penururnan which requires a continuous and gradual in the function, impaired function

social or work, and get rid penyebaba other dementia. 1,8,10,13

There are several criteria for clinical diagnosis of Alzheimer's disease are:

1. Criteria for diagnosis of suspected Alzheimer's disease consists of:

· Dementia established by clinical examination and mini mental status examination

or some similar examination and confirmed with a test neuropsikologik

· Obtained impaired cognitive function deficits> 2

• No disturbance of consciousness level

· Onset between the ages of 40-90 years, or often> 65 years

· There is no systematic abnormalities or other brain diseases.

2. Diagnosis of suspected Alzheimer's disease is supported by:

· Worsening progressive specific cognitive functions such as language, motor skills, and

perception

· ADL impaired and changes in behavior patterns

· A history of the family, especially if confirmed by neuropathology

· In the EEG provides a picture of a normal or nonspecific changes such as

increase in slow wave activity

· On CT scans obtained cerebral atrophy

3. Another picture of the suspect diagnosis of Alzheimer's disease after being expelled cause of

dementia

Other consists of:

· Symptoms associated with depression, insomnia, inkontinentia, delusions, hallucinations,

emotional, sexual disorders, weight loss

· Other neurological disorders in some patients, especially at an advanced stage of disease

and including motor signs such as increased muscle tone, myoclonus or

There is a rise of interference runs at an advanced stage

4. Picture of the suspect diagnosis of Alzheimer's disease is not clearly consist of:

· Onset of sudden

· Found focal neurologic symptoms such as hemiparese, hipestesia, roomy deficit

view and coordination problems

· There is a resurrection or walking at the time of onset disorders

5. Possible clinical diagnoses of Alzheimer's disease are:

· Dementia syndrome, there is no other neurologic symptoms, psychiatric symptoms or

disorders

systemic causes of dementia

· The existence of a secondary systemic disorders or abnormalities of the brain that causes

dementia,

severe cognitive deficits identified a gradual progressive

· There is no other cause

6. Criteria for definite diagnosis of Alzheimer's disease is a combination of clinical criteria for

suspect

Alzheimer's disease and histopathological images obtained from biopsy or autopsy.

2.9 Management

Treatment of Alzheimer's disease is still very limited because of the causes and

pathophysiological

remains unclear. Symptomatic and supportive treatment as if only to give a sense of satisfaction

in patients and families. Provision of stimulant medications, vitamins B, C, and E do not have

menguntungkan.10 effect, 11,12,14

1. Cholinesterase inhibitors

In recent years, many researchers use an inhibitor for the treatment

symptomatic Alzheimer's disease, where patients with Alzheimer's found decreased levels of

acetylcholine. To prevent a decline in acetylcholine levels can be used anti-cholinesterase

centrally acting like fisostigmin, THA (tetrahydroaminoacridine). Drug delivery

This is said to improve memory danapraksia during the last administration. Some

Researchers claim that the medicines will worsen the appearance of anti-cholinergic

intellectuals in normal people and patients with Alzheimer's. Drugs - drugs of this class that can

be

given, among others, 5-10 mg donepezil, rivastigmine and galantamine 6-12 mg 8-24 mg.

2. Thiamin

Research has shown that in people with Alzheimer's found a decrease thiamin

pyrophosphatase ketoglutarate dependent enzyme that is 2 (75%) and transketolase (45%), this

caused neuronal damage in the nucleus of thiamin basalis.Pemberian hydrochlorida with

dose of 3 g / day for 3 months peroral, showed significant improvement of function

cognition compared to placebo during the same period.

3. Nootropik

Nootropik is a psychotropic drug, has been proven to improve cognitive function and

learning process in experimental animals. But the provision of 4000 mg in patients with

Alzheimer's

did not show a clinically meaningful improvement.

4. Clonidine

Impaired intellectual function in patients with Alzheimer's can be caused by damage to

noradrenergic

cortical. Giving Clonidine (catapres) which is a noradrenergic alpha 2 receptor agonist

with a maximum dose of 1.2 mg orally for 4 weeks, showed a less

satisfactory to improve cognitive function

5. Haloperiodol

In people with Alzheimer's, psychosis disorder often occurs (delusions, hallucinations) and

behavior

behavior. Haloperiod oral administration of 1-5 mg / day for 4 weeks will improve the

symptoms

them. When Alzheimer's patients suffer from depression should be given tricyclic anti depresant

(Amitryptiline 25-100 mg / day)

6. Acetyl L-Carnitine (ALC)

Is an endogenous subtrate synthesized within the mitochondria with the aid of enzymes

ALC transferase. This study shows that ALC can increase the activity of acetyl

cholinesterase, choline acetyltransferase. In giving a dose of 1-2 g / day / orally for 1 year in

treatment, it was concluded that can improve or inhibit the progression

damage to cognitive function.

2:11 Prognosis

From examination of 42 patients with probable Alzheimer's clinical show that the prognostic

value

depends on three factors:

1. The degree of severity of illness

2. Variability of the clinical picture

3. Individual differences such as age, family dementia and sex

These three factors are tested statistically, was the first factor that most affects

prognostic patients with Alzheimer's. Patients with Alzheimer's disease have expectancy

The average life 4-10 years after diagnosis, and usually died of infection

secondary, such as pneumonia.

Measures Handling / Management

Treatment of Alzheimer's disease is still very limited because of the causes and pathophysiological still unclear. Symptomatic and supportive treatment as if only to give a sense of satisfaction in patients and families.

Symptomatic treatment:

1) cholinesterase inhibitors

    Objective: To prevent a decline in anti-acetylcholine levels can be used centrally acting cholinesterase    Example: fisostigmin, THA (tetrahydroaminoacridine), donepezil (Aricept), galantamin (Razadyne), & rivastigmin    Drug administration is said to improve memory and apraxia during the last administration    ESO: worsen the appearance of the intellectual in normal people and patients with Alzheimer's disease, nausea & vomiting, bradycardia, HCl ↑, and ↓ appetite.

2) Thiamin

In people with Alzheimer's found a decrease of thiamin pyrophosphatase ketoglutarate dependent enzyme that is 2 (75%) and transketolase (45%), this is due to neuronal damage in the nucleus basalis.

Example: thiamin hydrochloride

Dose of 3 g / day for 3 months peroral

Purpose: significant improvement of cognitive function compared to placebo during the same period.

3) Nootropik

    Nootropik is a psychotropic drug.    Objective: to improve the function of cognition and learning. But the provision of 4000 mg in patients with Alzheimer's disease showed no significant clinical improvement.

4) Clonidine

Impaired intellectual function in patients with Alzheimer's can be caused by damage to cortical noradrenergic.

    Example: Clonidine (catapres) which is an alpha 2 noradrenergic receptor agonist

    Dose: maximum 1.2 mg orally for 4 weeks    The goal: less than satisfactory for improving the cognitive functions

5) Haloperiodol

In people with Alzheimer's, often occur:

    Disorder psychosis (delusions, hallucinations) and behavior: Giving Oral Haloperiodol 1-5 mg / day for 4 weeks will improve the symptoms    When Alzheimer's patients suffer from depression gave tricyclic anti depresant (amitryptiline 25-100 mg / day)

6) Acetyl L-Carnitine (ALC)

Is an endogenous substrate is synthesized within the mitochondria with the help of ALC transferase enzymes.

    Objective: increase the activity of acetyl cholinesterase, choline acetyltransferase.    Dose :1-2 g / day / orally for 1 year in treatment        Effect: repairing damage or inhibit the progression of cognitive function (Yulfran, 2009)