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

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brain extracts, cell lysates
Species Reactivity
Intended Use
BACE1 ELISA is used to measure BACE1 in brain extracts or cultured cell lysate.
Contents of Kit
1. Precoated plate: Anti-BACE1 (N42) Rabbit IgG Affinity Purify. 96 Wells x 1
2. Labeled antibody Conc.: (30X) HRP conjugated Anti-BACE1 (C) Rabbit IgG Fab' Affinity Purify. 0. 4 mL x 1
3. Standard: Human BACE1 COS-7 Lysate. 0.5 mL x 2
4. EIA buffer. 30 mL x 1
5. Solution for Labeled antibody: 1% BSA, 0.05% Tween 20 in PBS. 12 mL x 1
6. Chromogen: TMB solution. 15 mL x 1
7. Stop solution: 1N H2SO4. 12 mL x 1
8. Wash buffer Conc.: (40X) 0.05% Tween 20 in phosphate buffer. 50 mL x 1
Storage Condition: 2-8°C. For more detailed information, please download the following document on our website.
Detection Range
1.56-100 ng/mL
0.16 ng/mL


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Beta-Amyloid-Dependent miRNAs as Circulating Biomarkers in Alzheimer's Disease: a Preliminary Report


Authors: Hajjri, Seyedeh Nazanin; Sadigh-Eteghad, Saeed; Mehrpour, Masoud; Moradi, Fatemeh; Shanehbandi, Dariush; Mehdizadeh, Mehdi

MicroRNAs (miRNAs) are considered among the most reliable biomarkers to diagnose and predict Alzheimer's disease (AD), due to their regulatory nature. The main goal of this study was to evaluate the expression of miR4422 and miR3714, as the main regulators of GSAP and BACE1 expression, in AD patients compared with healthy subjects. Twenty patients with a mild to moderate AD (58-71 years old) and 15 healthy subjects (58-73 years old) participated in this study. The expression levels of miR4422 and miR3714 as the target genes and 5S rRNA and miRlet7a-5p as the reference genes were measured in the two groups. To compare the expression between the case and the control groups, the t test or the Wilcoxon test was used, based on the data distribution patterns. The efficiencies of amplification of the miR4422, miR3714, 5S rRNA, and miRlet7a-5p genes all were in the acceptable range. The mean miR4422-5S rRNA dCt value was significantly different between the two groups (p = 0.018). The relative fold change of the expression was 0.43. The mean miR4422-miRlet7a-5p dCt value (p = 0.41), the mean miR3714-5S rRNA dCt value (p = 0.10), and the mean miR3714-miRlet7a-5p dCt value (p = 0.063) were not significantly different between the two groups. We indicated that miR4422 could be a reliable biomarker for Alzheimer's diagnosis. It seems that the reduced expression of miR4422 that targets GSAP and BACE1 expression can lead to an increase in the formation of A beta plaque.

Activation of Inflammation is Associated with Amyloid-beta Accumulation Induced by Chronic Sleep Restriction in Rats


Authors: Liu, Peng; Zhao, Beiyu; Wei, Meng; Li, Yanbo; Liu, Jie; Ma, Louyan; Shang, Suhang; Huo, Kang; Wang, Jin; Li, Rui; Qu, Qiumin

Alzheimer's disease (AD) is the most common age-associated neurodegenerative disease featured by progressive learning and memory deficit, and A beta was identified as playing a key role in the process of AD and was theorized to be caused by the imbalance of production and clearance. Increasing evidence suggested an association between sleep deprivation and AD. Our recent study found that chronic sleep restriction (CSR) caused cognitive impairment and A beta accumulation in rats, but the underlining mechanism was unclear. In the present study, we investigated the effects of inflammation on A beta accumulation induced by CSR. We found that CSR significantly increased the expression of interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), inducible nitric oxide synthase (iNOS), and nitric oxide (NO) in brain, and the inflammatory factors levels were positively correlated with A beta(42) deposition. Additionally, the inflammatory factors were correlated with BACE1, LRP-1, and RAGE levels in both the hippocampus and the prefrontal cortex. Furthermore, the plasma levels of IL-1 beta, TNF-alpha, and NO were elevated after CSR, and the concentration of plasma inflammatory mediators were correlated with plasma levels of sLRP1 and sRAGE. These results suggested that the inflammation in brain and plasma might be involved in the CSR-induced A beta accumulation.

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