Cellular basis of Alzheimers disease

被引：14

作者：

Bali, Jitin ^{[1
]}

Ben Halima, Saoussen ^{[1
]}

Felmy, Boas ^{[1
]}

Goodger, Zoe ^{[1
]}

Zurbriggen, Sebastian ^{[1
]}

Rajendran, Lawrence ^{[1
]}

机构：

[1] Univ Zurich, CH-8008 Zurich, Switzerland

来源：

ANNALS OF INDIAN ACADEMY OF NEUROLOGY | 2010年 / 13卷

关键词：

Alzheimers disease; amyloid precursor protein; beta-secretase; secretase; amyloid; trafficking; endocytosis; exosomes; AMYLOID PRECURSOR PROTEIN; PAIRED HELICAL FILAMENTS; BETA-SECRETASE; LIPID RAFTS; ASSOCIATION; CHOLESTEROL; TAU; CLEAVAGE; DEPENDS; PRIONS;

D O I：

10.4103/0972-2327.74251

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

Alzheimers disease (AD) is the most common form of neurodegenerative disease. A characteristic feature of the disease is the presence of amyloid- (A) which either in its soluble oligomeric form or in the plaque-associated form is causally linked to neurodegeneration. A peptide is liberated from the membrane-spanning -amyloid precursor protein by sequential proteolytic processing employing - and -secretases. All these proteins involved in the production of A peptide are membrane associated and hence, membrane trafficking and cellular compartmentalization play important roles. In this review, we summarize the key cellular events that lead to the progression of AD.

引用

页码：89 / 93

页数：5

共 40 条

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