Amyloid-β Peptides, Alzheimer's Disease and the Blood-brain Barrier

被引:59
作者
Gosselet, Fabien [1 ,2 ,3 ]
Saint-Pol, Julien [1 ,2 ,3 ]
Candela, Pietra [1 ,2 ,3 ]
Fenart, Laurence [1 ,2 ,3 ]
机构
[1] Univ Lille Nord France, Lille, France
[2] LBHE, EA 2465, Lens, France
[3] IMPRT IFR114, Lille, France
关键词
A beta peptides; ABC transporters; Alzheimer's disease; blood-brain barrier; brain capillary endothelial cells; brain pericytes; INSULIN-DEGRADING ENZYME; GLYCATION-END-PRODUCTS; CAPILLARY ENDOTHELIAL-CELLS; RECEPTOR-RELATED PROTEIN-1; TRANSGENIC MOUSE MODEL; SMOOTH-MUSCLE-CELLS; IN-VITRO MODEL; GAMMA-GLUTAMYL-TRANSPEPTIDASE; ANGIOTENSIN-CONVERTING ENZYME; TO-BASOLATERAL TRANSPORT;
D O I
10.2174/15672050113106660174
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Ever since amyloid-beta (A beta) peptides were first identified in cerebral plaques in patients with Alzheimer's disease (AD), much research work has focused on the complex mechanisms through which these peptides are synthesized, transported and degraded. Although new information emerges on a regular basis, we consider that the importance of the blood-brain barrier (BBB) in the pathogenesis of AD has been underestimated. In fact, there are a number of obstacles that make it difficult to convince specialists in AD that the BBB indeed plays a key role in this disease: these include the complex physiology of the BBB and the technical difficulty of studying the barrier in vivo and reproducing its main properties in vitro. With these considerations in mind, the present review sets out summarize our current knowledge about the physiology of the BBB and describe recent research findings on the barrier's role in A beta peptide proteostasis and thus in the mechanism of AD.
引用
收藏
页码:1015 / 1033
页数:19
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