Evidence suggests a link between Late Onset

It is a primary degenerative indisposition of the cerebral cortex. It accounts for everywhere 65% of all dementia cases, commonest cause of dementia. First described by Alzheimer in 1907 and named after him by Kraeplin. It is a forward whizz dam while. It destroys brain cells, causing problems with memory, thinking and behavior. The incidence is about 2 7 % at ages above 65yrs. This doubles after every additional 5yrs to 8-10% at 80yrs and 30-40% at 90yrs. R are below 50yrs. This progressive increase in incidence with age has caused significant medical, social and economic concerns in nations with growing number of elderly people.It is the 6th leading cause of death in the United States. It does not view any occurrent cure handling available is targeted at presenting symptoms. Pathology Aetiology The cause is unknown. However there is increased incidence in Downs syndrome. The risk is as well higher with increased informal radical formation and failure of antioxidant defens es which may contribute to the degeneration SOD is rock-bottom by 25% in the frontal cortex and hippocampus. It is occasionally familial. Besides, transmissible studies show connectorage surrounded by Familial AD and loci on chromosomes 1, 14 & 21.Late onset AD is a heterogenous disorder. Evidence suggests a link between Late Onset AD and atherosclerosis, inflammation and cholesterol. Linkage has in addition been found to a gene locus on chromosome 19q. There is too a strong association between Alzheimer disease and starchlike proteins. In this disease condition, there is a breakdown in some of the synapses that aid the function of information storage, processing and memory this riddles to other cells and over time, these cells die. such(prenominal) affected cells are surrounded by plaques and contain characteristic tangles.Macroscopy seeable examination of the brain shows a variable degree of cortical cachexia with widened sulci. These changes are pronounced in the front al, temporal and parietal lobes. Hydrocephalus ex vacuo -compensatory ventricular enlargement occurs due to parenchyma loss. Microscopy Microscopic examination shows senile plaques, neurofibrillary tangles and grainy angiopathy. All these changes are too found in the brains of elderly because they are features of aging. The pathologic changes seen in this disease begin first in the entorhinal cortex, spread to the hippocampus and isocortex and eventually to the neocortex.Senile plaques are spherical collections of dilate neuritic processes which surround a central amyloid core. The neuritic processes are also called dystrophic neuritis are silver-staining and contain polar helical filaments, kinky mitochondria and synaptic vesicles. The periphery is occupied by microglial cells and astrocytes. The amyloid core is stained by Congo red stain it contains abnormal proteins predominantly amyloid proteins. There are also diffuse plaques in those with Down syndrome these lack the neuri tic processes seen in senile plaques.Neurofibrillary tangles bundles of filaments in the cytoplasm of the neurons shape the nucleus. They are vivid as fibrillary structures with silver staining although they are also basophilic with Hematoxylin and Eosin stain. These structures contain paired helical and straight filaments the cause contain protein tau, Microtubule-associated protein MAP2 and ubiquitin. The quantities of these tangles correspond to the degree of dementia. Another pathologic feature is starchlike angiopathy which is an invariable finding in Alzheimer disease associated with amyloid protein.Besides, there is also accumulation of intraneuronal vacuoles in the cytoplasm. Amyloid angiopathy, hirano bodies are mostly within the frontal, parietal and temporal cortex, hippocampus and substantia inominata. There is also marked reduction in Ach, NE, 5-HT. Diagnosis Alzheimer disease usually becomes clinically apparent as insidious impairment of higher affable functions wi th changes in mood and behaviour. Later progressive impairment in orientation, memory, attention and concentration worsens.Eventually tolerant becomes mute, immobile and badly disturbed. The diagnosis of Alzheimer disease is based on a combination of clinical and pathologic presentations. There are impaired cognitive functions, Psychotic features such as delusion and hallucinations, and depression. The course is relentlessly progressive. Survival rate varies between 8 & 10yrs Management includes Good history, mental state and thorough fleshly examination. Every patient must be thoroughly evaluated to determine the finish and severity of the disease.Psychometric testing for confirmation, Mini Mental State Examination ,7-min screening, mental test score, clinical dementia rating, Wechsler adult intelligence scale WAIS current IQ to previous I Q Investigation these physiologic investigations are multipurpose to access the physical status of the patient identify any physical illn ess and determine co-morbidities. Blood test full haemogram, Erythrocyte depositary Rate, C-Reactive Protein, urea and electrolyte, Fasting and random blood sugar, liver function test, Ca, Vitamin B12, pteroylglutamic acid assay, Thyroid function test.Imaging Chest X-Ray, cranial CT scan, MRI, PET, SPECT, angiography Others Lumbar pierce and CSF analysis, brain biopsy for histology Treatment Generally, goal of treatment is to maintain remaining competency as far as possible to preserve dignity, relieve regretful symptoms, slow disease progression & provide care for as pine as possible in the familiar home environment. Patients should be do aware of their condition if possible. Inform patient the nature of the disease so that they can adapt favorably to existing conditions.Family support is an important begin of the treatment plan Counseling of the relatives & careers, family support and medical problems of the careers also deserve particular attention. The emphasis here is to encourage family members to show understanding for patients condition and help them live well with the condition. Behavioral methods that devour been suggested include re- enforcement, shaping, desensitization, prompts & other practical aids to cope with forgetfulness. Drug treatment there is not cure for Alzheimer disease but some drugs have proven useful in patients.These drugs are used based on their mechanism of action and the pathogenesis of the disease. These include Antioxidants these are useful to reduce allow radicals implicated as etiologic agents for AD. Anticholinesterases, such as neostigmine, physostigmine increase, Ach levels. Antipsychotics are indicated to subdue paranoid delusions while antidepressants may be indicated when depressive symptoms are prominent. Prevention youthful evidence suggests that participation in cognitively demanding activities in later spirit can be preventive. Prognosis The changes in Alzheimer disease are irreversible.The disease is terribly progressive and the biological history can rarely be altered. This makes the prognosis unfavorable. However, palliative measures can be adopted to alleviate the shortfall and preserve remaining functions. References Cummings J, Cole G Alzheimer Disease, JAMA 2872335, 2002 Braak H, Braak E frequence of Stages of Alzheimer-related lesions in different age categories. Neurobiol Aging 18351 1997 Braak H, Braak E Neuropahtological re-create of Alzheimer-related changes. Acta Neuropathol Berl 82239 1991 Mirra SM, Hart MN, Terry RD Making the diagnosis of Alzheimers disease. stiff Pathol Lab Med 117131, 1993