Insulin-degrading enzyme regulates the levels of insulin, amyloid β-protein, and the β-amyloid precursor protein intracellular domain in vivo
By Wesley Farris, Stefan Mansourian, Yang Chang, L. Lindsley, E. Eckman, Matthew P. Frosch, C. Eckman, Rudolph E. Tanzi, D. Selkoe, S. Guénette. Proceedings of the National Academy of Sciences of the United States of America, 2003
1,348 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Neurology, Physiology
View Paper: https://www.semanticscholar.org/paper/a02b9c002912f9eb1264da605253ebe394b51691
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Citations in the corpus
- The role of microglia in amyloid clearance from the AD brain (2010, methodology): “IDE has been reported to participate in Ab metabolism in vivo as genetically inactivation of the Ide gene in mice resulted in elevated levels of Ab in the brain and this effect was dependent on the gene dosage of Ide (Farris et al. 2003; Miller et al. 2003).”
- Decoding Alzheimer's disease from perturbed cerebral glucose metabolism: implications for diagnostic and therapeutic strategies. (2013, background): “…resistance such as mitogen-activated protein kinase (MAPK) pathway, GSK-3, insulin degrading enzyme (IDE) and microvascular dysfunction are responsible for AD pathophysiological alterations (Arab et al., 2011; Carro and Torres-Aleman, 2004; Dorr et al., 2012; Farris et al., 2003; Yan et al., 1996).”
- Mechanisms of insulin resistance in obesity (2013, background): “When these two molecules are deficient from gene inactivation in mice, insulin clearance will be blocked leading to hyperinsulinemia [74–76].”
- Physical activity and risk of neurodegenerative disease: a systematic review of prospective evidence (2008, background): “Beneficial effects of exercise on reducing amyloid b plaques in the frontel cortex have been demonstrated recently in a transgenic mouse model (Adlard et al. 2005 ; Lazarov et al. 2005), which might be mediated through insulin control (Farris et al. 2003).”
- Epidemiology of Alzheimer Disease (2012, neutral): “Type II Diabetes The presence of type II diabetes is associated with a approximately twofold increased risk of AD (risk ratios vary between 1.5 and 4.0; Luchsinger et al. 2001; Peila et al. 2002; Farris et al. 2003; Luchsinger et al. 2004a ).”
- ApoE promotes the proteolytic degradation of Abeta. (2008, background): “Mice in which Nep or Ide have been genetically inactivated exhibit higher Aβ levels and enhanced plaque deposition in the brain (Farris et al., 2003; Farris et al., 2007; Iwata et al., 2001).”
- Physical activity, including walking, and cognitive function in older women. (2004, neutral): “(%) 1261 (39) 1486 (43) 1516 (44) 1552 (44) 1463 (42)”