Remodelling of Ca2+ homeostasis in type I cortical astrocytes by hypoxia: evidence for association with Alzheimer's disease

Verfasser / Beitragende:
[C. Peers, I. F. Smith, J. P. Boyle, H. A. Pearson]
Ort, Verlag, Jahr:
2004
Enthalten in:
Biological Chemistry, 385/3-4(2004-04-13), 285-289
Format:
Artikel (online)
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024 7 0 |a 10.1515/BC.2004.023  |2 doi 
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245 0 0 |a Remodelling of Ca2+ homeostasis in type I cortical astrocytes by hypoxia: evidence for association with Alzheimer's disease  |h [Elektronische Daten]  |c [C. Peers, I. F. Smith, J. P. Boyle, H. A. Pearson] 
520 3 |a Sustained central hypoxia predisposes individuals to dementias such as Alzheimer's disease, in which cells are destroyed in part by disruption of Ca2+ homeostasis. Here, we show that exposure of astrocytes to hypoxia in vitro causes inhibition of plasmalemmal Na+/Ca2+ exchange and excessive mitochondrial Ca2q loading. Both factors disrupt normal agonist-evoked Ca2+ signalling. Moreover, hypoxia increases the levels of presenilin-1, a major component of a key enzyme involved in Alzheimers disease. Inhibition of this enzyme partially reverses the effects of hypoxia on Ca2+ signalling. These findings provide an initial cellular basis for understanding the clinical association of hypoxia with Alzheimers disease. 
540 |a Copyright © 2004 by Walter de Gruyter GmbH & Co. KG 
690 7 |a Biochemistry  |2 nationallicence 
690 7 |a Molecular biology  |2 nationallicence 
690 7 |a Cellular biology  |2 nationallicence 
700 1 |a Peers  |D C.  |4 aut 
700 1 |a Smith  |D I. F.  |4 aut 
700 1 |a Boyle  |D J. P.  |4 aut 
700 1 |a Pearson  |D H. A.  |4 aut 
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