Human BACE1(Beta-site APP Cleaving Enzyme 1) ELISA Kit (DEIA3191)

Regulatory status: For research use only, not for use in diagnostic procedures.

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Serum, plasma, tissue homogenates and other biological fluids.
Species Reactivity
Intended Use
BACE1 ELISA Kit allows for the in vitro quantitative determination of BACE1 concentrations in serum, plasma, tissue homogenates and other biological fluids.
Contents of Kit
2-8°C for 6 months
Intra-Assay: CV<8%
Inter-Assay: CV<10%
Detection Range
< 0.094ng/ml
Standard Curve


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Geraniin Attenuates Lipopolysaccharide-Induced Cognitive Impairment in Mice by Inhibiting Toll-Like Receptor 4 Activation


Authors: Wang, Dongmei; Dong, Xiaohui; Wang, Bei; Liu, Yumei; Li, Sanqiang

Geraniin has been reported to possess potent anti-inflammatory properties and to modulate the macrophage polarization. This study sought to evaluate the protective effects and underlying mechanisms of geraniin on lipopolysaccharide (LPS)-induced neuroinflammation and neurobiological alternations as well as cognitive impairment. Daily intragastrical administration with geraniin (20 mg kg(-1) day(-1)) for 14 days significantly prolonged the duration in the target quadrant (26.53 +/- 2.03 versus 37.09 +/- 3.27%; p < 0.05) and increased crossing-target number (1.93 +/- 0.22 versus 3.08 +/- 0.17; p < 0.01) in the probe test of LPS-treated mice. Geraniin also ameliorated LPS-elicited neural/synaptic impairments and decreased levels of LPS-induced A beta generation (p < 0.05), amyloid precursor protein (APP) (p < 0.05) and beta-site amyloid precursor protein cleavage enzyme 1 (BACE1) (p < 0.05). Furthermore, geraniin suppressed the production of pro-inflammatory cytokines, including tumor necrosis factor alpha (TNF-alpha) (9.85 +/- 0.58 versus 5.20 +/- 0.52 pg/mg of protein; p < 0.01), interleukin (IL)-1 beta (16.31 +/- 0.67 versus 8.62 +/- 0.46 pg/mg of protein; p < 0.01), and IL-6 (12.12 +/- 0.45 versus 7.43 +/- 0.32 pg/mg of protein; p < 0.05), and inhibited glial cell activation. Moreover, geraniin effectively polarized the microglia toward an anti-inflammatory M2 phenotype. Further study revealed that geraniin targeted toll-like receptor 4 (TLR4)-mediated signaling and decreased the production of pro-inflammatory cytokines in BV-2 microglial cells. These results indicate that geraniin mitigates LPS-elicited neural/synaptic neurodegeneration, amyloidogenesis, neuroinflammation, and cognitive impairment and suggest geraniin as a therapeutic option for neuroinflammation-associated neurological disorders, such as Alzheimer's disease.

Multitarget Approach to Drug Candidates against Alzheimer's Disease Related to AChE, SERT, BACE1 and GSK3 beta Protein Targets


Authors: Ivanova, Larisa; Karelson, Mati; Dobchev, Dimitar A.

Alzheimer's disease is a neurodegenerative condition for which currently there are no drugs that can cure its devastating impact on human brain function. Although there are therapeutics that are being used in contemporary medicine for treatment against Alzheimer's disease, new and more effective drugs are in great demand. In this work, we proposed three potential drug candidates which may act as multifunctional compounds simultaneously toward AChE, SERT, BACE1 and GSK3 beta protein targets. These candidates were discovered by using state-of-the-art methods as molecular calculations (molecular docking and molecular dynamics), artificial neural networks and multilinear regression models. These methods were used for virtual screening of the publicly available library containing more than twenty thousand compounds. The experimental testing enabled us to confirm a multitarget drug candidate active at low micromolar concentrations against two targets, e.g., AChE and BACE1.

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