Penyebab yang pasti belum diketahui.

Beberapa alternatif penyebab yang 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 terdiri dari degenerasi neuronal, kematian daerah spesifik jaringan otak yang mengakibatkan gangguan fungsi kognitif dengan penurunan daya ingat secara progresif. 10 Adanya defisiensi faktor pertumbuhan atau asam amino dapat berperan dalam kematian selektif neuron. Kemungkinan sel-sel tersebut mengalami degenerasi yang diakibatkan oleh adanya peningkatan calsium intraseluler, kegagalan metabolisme energi, adanya formasi radikal bebas atau terdapatnya produksi protein abnormal yang non spesifik. 11Penyakit alzheimer adalah penyakit genetika, tetapi beberapa penelitian telah membuktikan bahwa peran faktor genetika, tetapi beberapa penelitian telah membuktikan bahwa peran faktor non-genetika (lingkungan) juga ikut terlibat, dimana faktor lingkungan hanya sebagai pencetus faktor genetika. 1. Faktor genetik 2. 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 lingkungan Ekmann (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 imunologis Behan 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 trauma Beberapa 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 Neuropsikologik Always cause symptoms of Alzheimer's disease dementia. The function checks neuropsikologik is to determine the presence or absence of general cognitive dysfunction and find out in detail the pattern of deficit. Psychological test also aims to assess the function of the shown by some sections of different brain such as memory impairment, loss of expression, calculation, attention and understanding language. Neuropsychological evaluation Systematic has important diagnostic function because: 1. The existence of cognitive deficits associated with early dementia that can be known when minor changes that occur due to normal aging. 2. Neuropsikologik comprehensive examination allows to distinguish global cognitive disorders in dementia with selective deficits caused by

Focal dysfunction, metabolic factors, and psychiatric disorders 3. 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 with batrey use tool that manifests impaired cognitive function, which examination consists of: Verbal Fluency animal category Modified Boston naming test Mini-mental state Word list memory Constructional praxis Word list recall Word list recognition This test takes 30-40 minutes and <20-30 minutes in control. 3. CT Scan and MRI Is a non-invasive method of high resolution to see the quantification of changes volume 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 as multiinfark and cerebral tumors. Overall cortical atrophy and ventricular enlargement are both is the dominant image of a highly specific marker in this disease. But the picture It is also found in other dementias such as multiinfark, Parkinson's disease, Binswanger so it is hard to distinguish from Alzheimer's disease. Thinning of the cerebral substantia alba and ventricular enlargement correlated with the severity of symptoms clinics and mini-mental status examination. On MRI found an increase in intensity in cortical regions and periventrikuler (Capping the anterior horn in the lateral ventricles). Capping This is a predilection for early dementia. In addition to abnormalities found in cortical, picture atrophy was also seen in subcortical areas such as the atrophy of the hippocampus, amygdala, and sisterna basal enlargement and fissures sylvii. Seab et all, states are more sensitive MRI to distinguish dementia from Alzheimer's disease with other causes, taking into account the size (atrophy) of the hippocampus. 4. EEG Useful to identify activities that suklinis resurrection. Being on the disease Alzheimer changes in slow-wave obtained in a non-specific frontal lobe 5. PET (Positron Emission Tomography) In people with Alzheimer's, PET results found decreased blood flow, O2 metabolism, and cerebral glucose area. Up take I.123 greatly decreased in the parietal region, these results are very correlated with cognitive dysfunction and always and in accordance with observations neuropathology studies. 6. SPECT (Single Photon Emission Computed Tomography) Activity I. 123 ratio was lowest in patients with Alzheimer's parieral. These abnormalities correlated with extent of damage and functional deficits kogitif. Both of these checks (SPECT and PET) are not used routinely.

7. Laboratory blood No specific laboratory tests in patients with Alzheimer's. Examination this laboratory only to rule out other causes of dementia such as routine 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)