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• W2416283598 abstract "Advances in medicine are giving rise to extended life expectancy and thus diseases which usually affect the elderly popUlation will increase in prevalence. Alzheimer's disease (AD), the leading cause of dementia in the aged population, is devastating to the patients as well as their family members. This is a costly disease to the individuals and to society. Although an enormous effort is being made to understand the cause of this disease and to develop therapies for it, AD remains one of the foremost challenges to medical research today. The dementia occuring in AD is associated with dysfunction and death of neurons in a variety of cell populations, including cholinergic, monoaminergic, and peptidergic systems 1-3. A substantial amount of data support a central role of acetylcholine (ACh) in the cognitive dysfunction seen in AD and aging. Cerebral cortical ACh synthesis declines as a function of age in animals4,5. One of the earliest observed neurochemical changes in AD is the profound loss of neocortical cholinergic innervation.6--9 This loss has been found to be correlated with the degree of dementia found in the disease. Lesioning of cholinergic cell bodies in the nucleus basilis magnocellularis projecting to the neocortex induces marked deficits in cognitive performance in experimental animals3,10,1l and these cognitive deficits can be attenuated by cholinergic agonists, ACh releasing agents, and acetylcholinesterase inhibitors.2,12 These observations have led to what has been called the cholinergic hypothesis of AD which suggests that the cholinergic losses observed in AD lead directly to the cognitive and memonic deficits observed in the disease. However, with the wide range of neurochemical alterations now documented in ADI3--15 the cholinergic hypothesis appears to be an oversimplification. Strategies to enhance cholinergic function in brain (e.g. precursor loading, acetylcholinesterase inhibitors, and cholinergic receptor agonists) represent the predominant approaches that are currently being clinically evaluated to reverse some of the cognitive deficits seen in AD (for a review see Davis et al. I6). Precursor loading with choline or phosphatidylcholine failed to have a significant effect on AD symptoms. 17,18 Treatment with acetylcholinesterase inhibitors such as physostigmine 19,20 and tetrahydroaminoacridine 21,22 to retard the degrada-" @default.
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• W2416283598 modified "2023-09-24" @default.
• W2416283598 title "A Depolarization-Activated Releaser of Transmitters for Treatment of Dementia" @default.
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