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Alzheimers Dementia is a progressive and degenerative dementia whose underlying cause is still a mystery. It affects 11% of the population in the United States over the age of 65, and almost half of all people over 85. Throughout the course of this disease, patients exhibit a progressive loss of all their higher cognitive functions including memory, language, and perception.
Several drugs, such as Warner Lambert's Cognex (Tacrine) and Pfizer's Aricept (Donepezil), have recently been introduced for patients with Alzheimers Dementia. These drugs work by enhancing the efficacy of the cholinergic cells which are known to be depleted in patients with Alzheimers Dementia. Although these drugs act to slow the progression of the symptoms of the disease, it is unclear whether or not they slow down the disease itself. Numerous other drugs currently under development may hold the promise for greater efficacy in slowing the progression of functional deficits. It is important to realize, however, that there is no known cure for Alzheimers Dementia, and few researchers expect that we will ever be able to substantially reverse the cognitive deficits that have already occurred in a patient with Alzheimers Dementia. As neuronal connections wither and die in these patients, they take with them the summed effect of years of experience and learning that can never be replicated or replaced. Thus, the only realistic hope for preventing cognitive losses through the application of drugs is by diagnosing patients in the very earliest stages of Alzheimers Dementia, before they suffer from the dramatic functional consequences which result from many lost neuronal connections.
Two different aspects of our work relate to memory loss (and enhancement) in normal aging and in Alzheimers Dementia, and we turn now to discuss them.