Amyloid β-peptide and Alzheimer's disease

被引:0
作者
Allsop, David [1 ]
Mayes, Jennifer [1 ]
机构
[1] Univ Lancaster, Div Biomed & Life Sci, Fac Hlth & Med, Lancaster LA1 4YQ, England
来源
AMYLOIDS IN HEALTH AND DISEASE | 2014年 / 56卷
基金
英国惠康基金;
关键词
amyloid cascade; genetics; oligomer; secretase; senile plaque; treatment; MILD COGNITIVE IMPAIRMENT; PRECURSOR PROTEIN; BINDING DOMAIN; SECRETASE; COPPER; DEPOSITION; MUTATION; ALLELE; APP;
D O I
10.1042/BSE0560099
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
One of the hallmarks of AD (Alzheimer's disease) is the formation of senile plaques in the brain, which contain fibrils composed of A beta (amyloid beta-peptide). According to the 'amyloid cascade' hypothesis, the aggregation of A beta initiates a sequence of events leading to the formation of neurofibrillary tangles, neurodegeneration, and on to the main symptom of dementia. However, emphasis has now shifted away from fibrillar forms of A beta and towards smaller and more soluble 'oligomers' as the main culprit in AD. The present chapter commences with a brief introduction to the disease and its current treatment, and then focuses on the formation of A beta from the APP (amyloid precursor protein), the genetics of early-onset AD, which has provided strong support for the amyloid cascade hypothesis, and then on the development of new drugs aimed at reducing the load of cerebral A beta, which is still the main hope for providing a more effective treatment for AD in the future.
引用
收藏
页码:99 / 110
页数:12
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