Prion protein in Alzheimer's pathogenesis: a hot and controversial issue

被引：33

作者：

Benilova, Iryna ^{[1
,2
]}

De Strooper, Bart ^{[1
,2
]}

机构：

[1] Flanders Inst Biotechnol VIB, Dept Mol & Dev Genet, Louvain, Belgium

[2] KULeuven, Ctr Human Genet, Louvain, Belgium

来源：

EMBO MOLECULAR MEDICINE | 2010年 / 2卷 / 08期

关键词：

Amyloid-beta (A beta); oligomers; A beta receptor; prion protein (PrP); neurotoxicity; AMYLOID-BETA OLIGOMERS; DISEASE; IMPAIRMENT; BIOLOGY; MICE;

D O I：

10.1002/emmm.201000088

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

100103 [病原生物学]; 100218 [急诊医学];

摘要：

The role for cellular prion protein PrPc in beta-amyloid (A beta) oligomer-induced synaptic impairment is a topic of great interest and some controversy. In this issue of EMBO Molecular Medicine Aguzzi and co-workers explore the contribution of PrPc to deficient long term potentiation (LIP) and soluble All levels in an Alzheimer's disease mouse model and show that the role of prions in A beta related toxicity is far from 'black and white' suggesting complex interpretations of the data available thus far.

引用

页码：289 / 290

页数：2

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