期刊
JOURNAL OF THE KOREAN MEDICAL ASSOCIATION
卷 52, 期 11, 页码 1059-1068出版社
KOREAN MEDICAL ASSOC
DOI: 10.5124/jkma.2009.52.11.1059
关键词
Alzheimer's disease (AD); Disease modifying therapy; Amyloid; Hyperphosphorylated tau
Alzheimer disease (AD) is pathologically characterized by extracellular amyloid deposits composed of beta-amyloid (A beta) peptide, neurofibrillary tangles (NFTs) made up of hyperphosphorylated tau, and deficit of cholinergic neurons in the basal forebrain. It is the most common neurodegenerative disease in the elderly. With the aging of the population, the incidence and prevalence of AD will also increase rapidly. The subsequent growing socioeconomic burden seems to be inevitable until effective therapeutic strategies are developed. Currently available treatments approved by the US Food and Drug Administration, while ameliorating the symptoms, do not halt progression or cure the illness. AD is a multifactorial syndrome with several target proteins contributing to its etiology. In this review, various small molecules targeting pathological hall marks or their major constituents that have been reported in the literature will be discussed, with emphasis on compounds that are presently being investigated in clinical trials.
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