Hypoxia facilitates Alzheimer's disease pathogenesis by up-regulating BACE1 gene expression

By Xiulian Sun, G. He, H. Qing, Weihui Zhou, Frederick A. Dobie, Fang Cai, M. Staufenbiel, L. E. Huang, Weihong Song. Proceedings of the National Academy of Sciences of the United States of America, 2006

637 citations recorded by the source corpus.

Subfields: Molecular Biology, Neurology, Physiology

View Paper: https://www.semanticscholar.org/paper/5b80e4aa0234574c8a277bf02c6b82933345ba9b

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. J. Long
2. David Attwell
3. D. Holtzman
4. C. Iadecola
5. Berislav Zlokovic

In Neurology

1. C. Iadecola
2. J. Long
3. David Attwell
4. D. Holtzman
5. Berislav Zlokovic

In Physiology

1. J. Long
2. C. Iadecola
3. David Attwell
4. D. Holtzman
5. Berislav Zlokovic

Citations in the corpus

• The pathobiology of vascular dementia (2013, positive): “Ab Production and Clearance Hypoperfusion and hypoxia caused by vascular insufficiency may also facilitate Ab production by activating the APP cleavage enzyme b-secretase (Kitaguchi et al., 2009; Sun et al., 2006; Tesco et al., 2007; Wen et al., 2004a).”
• Alzheimer Disease: An Update on Pathobiology and Treatment Strategies (2019, positive): “Hypoxia can induce increased Aβ production, possibly via increased BACE1 expression (Sun et al., 2006), suggesting the possibility of a pathological feedforward loop.”
• Amyloid β oligomers constrict human capillaries in Alzheimer’s disease via signaling to pericytes (2019, background): “This in turn increases Ab production by up-regulating b-amyloid–converting enzyme (BACE1, also called b-secretase 1) (13, 14).”