Regular ArticleLocalization of β-Secretase Memapsin 2 in the Brain of Alzheimer's Patients and Normal Aged Controls
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Neuronal expression of ILEI/FAM3C and its reduction in Alzheimer's disease
2016, NeuroscienceCitation Excerpt :Moreover, APP and components of the γ-secretase complex exhibited co-localization with ILEI. The putative major site of Aβ generation in the brain is synaptic terminals, although immunostaining for APP, BACE1 (β-secretase), and γ-secretase complex components did not reveal a synaptic pattern (Lee et al., 1996; Lah et al., 1997; Sun et al., 2002). Subcellular fractionation using mouse brain showed an overlapping distribution of synaptophysin and ILEI (Fig. 3B).
Decrease in catalytic capacity of γ-secretase can facilitate pathogenesis in sporadic and Familial Alzheimer's disease
2015, Molecular and Cellular NeuroscienceCitation Excerpt :Therefore, such measurements can be directly related to the pathogenic changes in Aβ products and Aβ 42/40 ratio according to differences in the Michaelis–Menten constant for each product (Kakuda et al., 2006; Svedruzic et al., 2013; Yin et al., 2007). The results in Figs. 1–3 are consistent with the previous studies on humans, experimental animals, cells, and enzymes which showed that pathogenic events correlate with increase in saturation of γ-secretase with its substrate or decrease in its maximal activity (Fukumoto et al., 2004; Jonsson et al., 2012; Holsinger et al., 2004; Li et al., 2004; Sun et al., 2002; Yang et al., 2003; Guyant-Marechal et al., 2007; Rovelet-Lecrux et al., 2006, 2007; Citron et al., 1992; Cai et al., 1993; German and Eisch, 2004; Marlow et al., 2003; Refolo et al., 1999; Svedruzic et al., 2012, 2013). For example, we find earlier “age-of-onset” and “age-of-death” with the less active (Fig. 1), more saturated FAD mutants (Fig. 2), that have lower capacity to process their β-CTF-APP substrate (Fig. 5).
Shared cognitive and behavioral impairments in epilepsy and Alzheimer's disease and potential underlying mechanisms
2013, Epilepsy and BehaviorCitation Excerpt :Indeed, mouse models in which β subunits of voltage-gated sodium channels are ablated or mutated exhibit a predisposition to seizures [48–52]. Notably, BACE1 levels are increased in the brains of patients with AD and hAPP mouse models of AD [48,53–60], and the magnitude of the increase is correlated with increased β2 subunit cleavage in the brains of patients with AD [48]. These studies suggest that BACE1-mediated cleavage of the β2 subunit may contribute to AD-related increase in principal cell activity, although this has yet to be determined.
The miR-124 regulates the expression of BACE1/β-secretase correlated with cell death in Alzheimer's disease
2012, Toxicology LettersCitation Excerpt :The expression of miR-124 is enriched in neurons but not astrocytes, and its expression level increased over time in the developing nerve system (Krichevsky et al., 2003; Miska et al., 2004; Makeyev et al., 2007; Smirnova et al., 2005;). Moreover, it has been reported that the expression of miR-124 is down-regulated in the brains of patients with AD while the expression of BACE1 is up-regulated in these patients (BigI et al., 2000; Holsinger et al., 2002; Lukiw, 2007; Sun et al., 2002; Smith et al., 2011; Yang et al., 2003). Hence, in order to address the role and target gene regulation network of miR-124 in cellular AD model induced by Aβ1-42 neurotoxicity, we tested in vitro miRNA gain and loss of function in cellular AD model, elucidated the expression alteration of one of its potential downstream targets, BACE 1, and the profiles of cell death and survival following treatments with mimics or inhibitor of miR-124.
Enhanced activity of hippocampal BACE1 in a mouse model of postmenopausal memory deficits
2008, Neuroscience Letters
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To whom correspondence should be addressed at Department of Anatomy & Neurobiology, University of Kentucky Medical Center, Room 310, Davis-Mills Building, 800 Rose Street, Lexington, KY 40536. Fax: (859) 257-3625. E-mail: [email protected].