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KMID : 1100220050040020053
Dementia and Neurocognitive Disorders
2005 Volume.4 No. 2 p.53 ~ p.58
Molecular Targets for the Treatment of Alzheimer¡¯s Disease
Han Seol-Heui

Abstract
Alzheimer¡¯s disease (AD) is regarded as a prototype of the neurodegenerative disorder characterized by progressive memory impairment and multiple cognitive deficits in mid to late life. Its pathological hallmarks consist of neuritic plaques and neurofibrillary tangles in the cerebral cortex, accompanied by neuronal loss. These neuropathological findings are prominent in the temporal neocortex and hippocampus. There are a small proportion of AD cases(~10%) that appear to be transmitted as pure autosomal dominant. Mendelian traits with agedependent but high penetrance. Molecular genetic studies on pedigrees with the latter type of familial Alzheimer¡¯s disease (FAD) with molecular genetic tools have led to the discovery of four different genetic loci associated with inherited susceptibility to AD. It is generally suggested that late-onset AD is caused by a complex set of genetic and environmental factors, such as diet, blood pressure, education, social interaction, and others. In this communication, some of the known risk factors relevant to etiopathogenesis of Alzheimer¡¯s disease to date will be briefly reviewed.
KEYWORD
Alzheimer¡¯s disease, Etiopathogenesis, Amyloid cascade hypothesis, Risk factors, Therapeutic targets
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