Evidence suggests a link between Late Onset

It is a primary degenerative disease of the cerebral cortex. It accounts for over 65% of all dementia cases, commonest cause of dementia. First described by Alzheimer in 1907 and named after him by Kraeplin. It is a progressive brain damage. 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. Rare 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 have any current cure; treatment available is targeted at presenting symptoms. Pathology Aetiology: The cause is unknown. However there is increased incidence in Down’s syndrome. The risk is also higher with increased free radical formation and failure of antioxidant defenses which may contribute to the degeneration [SOD is reduced by 25% in the frontal cortex and hippocampus]. It is occasionally familial. Besides, genetic studies show linkage between 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 also been found to a gene locus on chromosome 19q. There is also a strong association between Alzheimer disease and amyloid proteins. In this disease condition, there is a breakdown in some of the synapses that serve the function of information storage, processing and memory; this spreads to other cells and over time, these cells die. Such affected cells are surrounded by plaques and contain characteristic tangles.
Macroscopy: Macroscopic examination of the brain shows a variable degree of cortical atrophy with widened sulci. These changes are pronounced in the frontal, temporal and parietal lobes. Hydrocephalus ex vacuo -compensatory ventricular enlargement occurs due to parenchyma loss. Microscopy: Microscopic examination shows senile plaques, neurofibrillary tangles and amyloid angiopathy. All these changes are also 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 paired helical filaments, abnormal 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 neuritic processes seen in senile plaques.
Neurofibrillary tangles: bundles of filaments in the cytoplasm of the neurons encircling 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 former contain protein tau, Microtubule-associated protein [MAP2] and ubiquitin. The quantities of these tangles correspond to the degree of dementia. Another pathologic feature is Amyloid 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 mental functions with changes in mood and behaviour. Later progressive impairment in orientation, memory, attention and concentration worsens.
Eventually patient becomes mute, immobile and severely 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 physical examination. Every patient must be thoroughly evaluated to determine the extent 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 physical investigations are useful to access the physical status of the patient; identify any physical illness and determine co-morbidities. Blood test : full haemogram, Erythrocyte Sedimentation Rate, C-Reactive Protein, urea and electrolyte, Fasting and random blood sugar, liver function test, Ca, Vitamin B12, Folate assay, Thyroid function test.
Imaging: Chest X-Ray, cranial CT scan, MRI, PET, SPECT, angiography Others: Lumbar Puncture and CSF analysis, brain biopsy for histology Treatment Generally, goal of treatment is to maintain remaining ability as far as possible to preserve dignity, relieve distressing symptoms, slow disease progression & provide care for as long as possible in the familiar home environment. Patients should be made 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 part 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 patient’s condition and help them live well with the condition. Behavioral methods that have 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 free radicals implicated as etiologic agents for AD. Anticholinesterases, such as neostigmine, physostigmine increase, Ach levels. Antipsychotics are indicated to control paranoid delusions while antidepressants may be indicated when depressive symptoms are prominent. Prevention: recent evidence suggests that participation in cognitively demanding activities in later life 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 deficit and preserve remaining functions. References Cummings J, Cole G: Alzheimer Disease, JAMA 287:2335, 2002 Braak H, Braak E: Frequency of Stages of Alzheimer-related lesions in different age categories. Neurobiol Aging 18:351; 1997 Braak H, Braak E: Neuropahtological staging of Alzheimer-related changes. Acta Neuropathol [Berl] 82:239; 1991 Mirra SM, Hart MN, Terry RD: Making the diagnosis of Alzheimer’s disease. Arch Pathol Lab Med 117:131, 1993

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