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Alzheimer's disease is the most common dementing disease in the industrialized countries affecting approximately one in five persons over the age of 80 years. It is characterized by memory loss, personality changes and signs of cortical malfunction such as apraxia, aphasia and agnosia. Substantial pathological changes have been found in cortical and subcortical areas, including neurofibrillary tangles and amyloid-containing neuritic plaques. The hippocampus appears to be particularly vulnerable to such changes, which probably accounts for the gross disturbance in memory function that occurs early in the onset of the disease.

Alzheimer's disease was first described in 1907 by Alois Alzheimer who identified and described the presence of numerous neurofibrillary tangles in the brain of a 51-year-old woman who had suffered from progressive dementia over a number of years. These neurofibrillary tangles were predominantly found in the hippocampus, amygdala, nucleus basalis, hypothalamus and several other subcortical structures. Further studies clearly showed that the density of those tangles correlated with the degree of cognitive impairment shown by the patient prior to death. The other characteristic pathological feature of the brain of the patient with Alzheimer's disease is the presence of senile or neuritic plaques. Such structures are large, lie within the neurophil, and occur throughout the neocortex and hippocampus. The density of these plaques is also correlated with the degree of cognitive impairment shown by the patient at the time of death. In addition to the tangles and plaques, Hirano bodies are also a feature of the post-mortem brain of the Alzheimer patient. These bodies were first

Fundamentals of Psychopharmacology. Third Edition. By Brian E. Leonard © 2003 John Wiley & Sons, Ltd. ISBN 0 471 52178 7

described in the brains of patients suffering from a rare dementing disease called amyotrophic lateral sclerosis of Guam (Figures 14.1, 14.2).

Gross changes are also apparent in the brain of an Alzheimer's patient, but do not appear to be specific for Alzheimer's disease. Thus the brain weight is reduced compared with age- and sex-matched non-demented individuals, although it must be emphasized that there is considerable overlap

Figure 14.1. Diagrammatic representation of a ß-amyloid protein plaque.
Figure 14.2. Diagrammatic representation of neurofibrillary tangles in neuron.

between the controls and demented patients. A moderate degree of lateral and third ventricular dilatation is also apparently associated with a thinning of the cortex. Loss of the underlying white matter also occurs in the brains of Alzheimer's patients. In contrast, the deeper subcortical nuclei of the basal ganglia and thalamus appear to retain their normal appearance (Figure 14.3).

Although it has been postulated that the presence of amyloid protein in the Alzheimer's brain could be specifically involved in the causation of the central sulcus postcentral gyrus parietal lobe

parietooccipital sulcus precentral gyrus cingulate gyrus frontal lobe calca rine sulcus

precentral gyrus cingulate gyrus frontal lobe nucleus of meynert

© CNSforu nucleus of meynert

Figure 14.3. Diagram of the areas of the brain primarily affected in patients with Alzheimer's disease. Q

disease, there is now evidence that amyloid deposits also occur in the brains of patients with other types of neurological disorder and it is therefore doubtful whether amyloid protein alone is a primary pathogenetic factor for this illness. However, it is also possible that the structure of the amyloid protein in the brain of the Alzheimer patient differs from that in the brain of the aged individual.

By definition, Alzheimer's disease (AD) is a progressive, degenerative disease of the brain that is the most common cause of dementia in the elderly. Post-mortem studies have demonstrated that the most common pathological features of AD are neuritic plaques and neurofibrillary tangles. By definition, all patients with AD must have dementia, a progressive loss of memory and at least one other defect in cognitive function which is sufficient to impede daily functioning. A clinical diagnosis of AD can only be made with certainty when no other situation can account for the progressive cognitive impairment.

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