Insulin-degrading enzyme regulates the levels of insulin, amyloid beta-protein, and the beta-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

751 citations recorded by the source corpus.

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Citations in the corpus

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).”
Aggregation of vascular risk factors and risk of incident Alzheimer disease (2005, background): “Insulin degrading enzyme in the brain is a regulator of extracellular amyloid beta levels (82,83) inhibited by insulin (83,84).”
Relation of diabetes to mild cognitive impairment. (2007, unknown): “Hyperinsulinemia, which can precede and accompany diabetes,(48) may disrupt brain amyloid clearance by means of the insulin degrading enzyme.(7) Another potential mechanism is the generation of advanced products of glycosylation.”
The role of microglia in amyloid clearance from the AD brain (2010, background): “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).”
Alzheimer’s disease prevention: from risk factors to early intervention (2017, background): “It has been suggested that diabetes could increase the risk by directly affecting Aβ accumulation in the brain since hyperinsulinemia disrupts brain Aβ clearance by competing for the insulin-degrading enzyme [12, 13].”
P-glycoprotein deficiency at the blood-brain barrier increases amyloid-beta deposition in an Alzheimer disease mouse model. (2005, background): “Aβ is secreted from neurons into brain interstitial fluid (ISF), where it is eliminated by proteolytic degradation (1, 2), passive bulk flow (3), and active transport across the blood-brain barrier (BBB) (4, 5).”
Physical activity and risk of neurodegenerative disease: a systematic review of prospective evidence (2008, background): “2005), which might be mediated through insulin control (Farris et al. 2003).”
Insulin Action in Brain Regulates Systemic Metabolism and Brain Function (2014, background): “Insulin and Ab are both substrates of insulin-degrading enzyme, and it has been suggested that hyperinsulinemia inhibits the degradation of Ab by competitively blocking insulin-degrading enzyme (91).”
ApoE promotes the proteolytic degradation of Abeta. (2008, background): “Genetic inactivation of these genes (Farris et al., 2003; Iwata et al., 2001) or administration of inhibitors of these proteinases into the brain results in substantial elevation of Ab levels in the brain and induction of plaque deposition (Dolev and Michaelson, 2004).”
Diet‐induced insulin resistance promotes amyloidosis in a transgenic mouse model of Alzheimer's disease (2004, background): “This relationship of IDE with Aβ is supported by recent evidence indicating that IDE activity in the brain is negatively correlated with Aβ content (7, 8), and that IDE expression is decreased in the AD brain (9, 10).”