Beta-secretase protein and activity are increased in the neocortex in Alzheimer disease.
By H. Fukumoto, B. Cheung, Bradley T. Hyman, M. Irizarry. Archives of Neurology, 2002
740 citations recorded by the source corpus.
View Paper: https://www.semanticscholar.org/paper/c8e3609c629bb4f3a9f7e84140ea41ef03b4b895
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- Wang-Xia Wang
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Citations in the corpus
- The Expression of MicroRNA miR-107 Decreases Early in Alzheimer's Disease and May Accelerate Disease Progression through Regulation of β-Site Amyloid Precursor Protein-Cleaving Enzyme 1 (2008, result): “Notwithstanding this technical shortcoming, the total number of miRNAs expressed above background is quite compatible with the previous findings of other brain miRNA microarray studies (Baskerville and Bartel, 2005; Gaur et al., 2007; Tang et al., 2007).”
- Oxidative Stress and the Pathogenesis of Alzheimer's Disease (2013, background): “…of Abeta and tau proteins in the induction of redox imbalance and the generation of free radicals throughmechanisms such as mitochondria dysfunction and/or transitionmetal homeostasis imbalance and discusses the mechanisms by which oxidative stress promotes Abetaand tau-mediated neurotoxicity.”
- Alzheimer’s Disease and the β-Amyloid Peptide (2010, unknown): “…effect shows a brain regional selectivity that roughly parallels disease affected regions and is related to both plaque burden and disease duration [45–47]. β -secretase activity has also been seen to increase with age in rodents and nonhuman primates [48], although these species do not develop AD.”
- Quantitative targeted absolute proteomics of human blood–brain barrier transporters and receptors (2011, background): “The protein levels have been shown to correlate to the activities of various functional membrane proteins, such as Na+/glucose cotransporter 1, cytochrome P450 2D6 (CYP2D6) and b secretase (Dyer et al. 1997; Fukumoto et al. 2002; Langenfeld et al. 2009).”