Antagonizing amyloid-β/calcium-sensing receptor signaling in human astrocytes and neurons: a key to halt Alzheimer's disease progression?

被引：22

作者：

Dal Pra, Ilaria ^{[1
]}

Chiarini, Anna ^{[1
]}

Armato, Ubaldo ^{[1
]}

机构：

[1] Univ Verona, Sch Med, Histol & Embryol Sect, Dept Life & Reprod Sci, I-37134 Verona, Venetia, Italy

来源：

NEURAL REGENERATION RESEARCH | 2015年 / 10卷 / 02期

关键词：

Alzheimer's disease; amyloid-beta; astrocytes; Ca2+; calcilytic; calcium-sensing receptor; nitromemantine; NPS; 2143; alpha 7-nicotinic acetylcholine receptor; CALCIUM; SECRETION; TARGET;

D O I：

10.4103/1673-5374.152373

中图分类号：

Q2 [细胞生物学];

学科分类号：

071013 [干细胞生物学];

摘要：

Astrocytes' roles in late-onset Alzheimer's disease (LOAD) promotion are important, since they survive soluble or fibrillar amyloid-beta peptides (A beta s) neurotoxic effects, undergo alterations of intracellular and intercellular Ca2+ signaling and gliotransmitters release via the A beta/alpha 7-nAChR (alpha 7-nicotinic acetylcholine receptor) signaling, and overproduce/oversecrete newly synthesized A beta(42) oligomers, NO, and VEGF-A via the A beta/CaSR (calcium-sensing receptor) signaling. Recently, it was suggested that the NMDAR (N-methyl-D-aspartate receptor) inhibitor nitromemantine would block the synapse-destroying effects of A beta/alpha 7-nAChR signaling. Yet, this and the progressive extracellular accrual and spreading of A beta(42) oligomers would be stopped well upstream by NPS 2143, an allosteric CaSR antagonist (calcilytic).

引用

页码：213 / 218

页数：6

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