Diverse Molecular Targets for Therapeutic Strategies in Alzheimer's Disease

被引:22
|
作者
Han, Sun-Ho [1 ]
Mook-Jung, Inhee [1 ]
机构
[1] Seoul Natl Univ, Coll Med, Dept Biochem & Biomed Sci, Seoul 110799, South Korea
关键词
Alzheimer Disease; Amyloid Beta-Peptides; Tau Protein; Immunotherapy; Glucose Metabolism; Aggregation; AMYLOID-BETA-PROTEIN; REVERSES COGNITIVE IMPAIRMENT; PLACEBO-CONTROLLED TRIAL; A-BETA; TRANSGENIC MICE; GAMMA-SECRETASE; MOUSE MODEL; SYNAPTIC PLASTICITY; GLUCOSE-METABOLISM; PRECURSOR PROTEIN;
D O I
10.3346/jkms.2014.29.7.893
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Alzheimer's disease (AD) is the most common form of dementia caused by neurodegenerative process and is tightly related to amyloid beta (A beta) and neurofibrillary tangles. The lack of early diagnostic biomarker and therapeutic remedy hinders the prevention of increasing population of AD patients every year. In spite of accumulated scientific information, numerous clinical trials for candidate drug targets have failed to be preceded into therapeutic development, therefore, AD-related sufferers including patients and caregivers, are desperate to seek the solution. Also, effective AD intervention is desperately needed to reduce AD-related societal threats to public health. In this review, we summarize various drug targets and strategies in recent preclinical studies and clinical trials for AD therapy: Allopathic treatment, immunotherapy, A beta production/aggregation modulator, tau-targeting therapy and metabolic targeting. Some has already failed in their clinical trials and the others are still in various stages of investigations, both of which give us valuable information for future research in AD therapeutic development.
引用
收藏
页码:893 / 902
页数:10
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