Alzheimer is mostly seen in individuals who are above the age of forty five and it principally develops into dementia in its latter stages. It is characterized by loss of cognitive abilities which occurs due to the loss of normal brain functions. In the latter stages of Alzheimer Disease the sufferer becomes totally disoriented and shows memory loss such that he is not able to recognize his very close family members. (Evans et al, 1989; Gao et al, 1999). The primary feature of Alzheimer Disease is the atrophy of the cortex. But in some cases it is seen that neuritic processes may accumulate, abnormalities in cerebral nucleus may occur or amyloid angiopathy may be seen.
It is seen that Alzhemier Disease does not show any symptoms early at age but after a person reaches 50 the symptoms become obvious. As an individual ages the chances of the disease increase even more often reaching to a level of 40% in individuals who are in their eighties ((Evans et al, 1989; Gao et al, 1999; Strauss et al 1999 ). Studies on the disease have shown that cortical atrophy is the major cause of the disease. The cerebral sulci become more prominent in the temporal, frontal and parietal lobes. To cover up for this atrophy usually the ventricle in the brain enlarges. Microscopic studies have shown that neuritic plaques and neurofibrillary tangles accumulate along with amyloid angiopathy. Neuritic plaques are spherical neuritic processes which surround the central amyloid core in Alzheimer. Neurofibrillary tangles are a group of filaments which are found in the cytoplasm of the neurons that usually surround the nucleus. Amyloid angiopathy is a sign of Alzhemier Disease but it can also be found in other diseases. It is believed that Alzheimer later progresses to dementia in individuals because of loss of choline accetyltransferase, synaptophysin immunoreactivity and loss of synaptic transmission. It is believed that Alzheimer is primarily caused by a protein known as Aβ. Aβ is