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aβ42 elisa kit  (Cusabio)


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    Cusabio aβ42 elisa kit
    Aβ42 Elisa Kit, supplied by Cusabio, used in various techniques. Bioz Stars score: 93/100, based on 33 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/a%CE%B242+elisa+kit/Human+amyloid+beta+peptide+1-42%2CA%CE%B21-42+ELISA+Kit/pm41126442-262-10-14
    Average 93 stars, based on 33 article reviews
    aβ42 elisa kit - by Bioz Stars, 2026-09
    93/100 stars

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    Related Articles

    Enzyme-linked Immunosorbent Assay:

    Article Title: Neuroprotective Effect of Ligustilide through Induction of α-Secretase Processing of Both APP and Klotho in a Mouse Model of Alzheimer’s Disease
    Article Snippet: .. The soluble and insoluble Aβ levels in all samples were determined using the commercially available mouse Aβ40 and Aβ42 ELISA kit (CUSABIO) according to manufacturer’s instructions. ..

    Article Title: Astaxanthin Improved the Cognitive Deficits in APP/PS1 Transgenic Mice Via Selective Activation of mTOR.
    Article Snippet: .. Astaxanthin (Ast) is an effective neuroprotective and antioxidant compound used to treat Alzheimer’s disease (AD); however, the underlying in vivomolecular mechanisms remain unknown.. In this study, we report that Ast can activate the mammalian target of rapamycin (mTOR) pathway in the 8-month-old APP/PS1 transgenic mouse model of AD.. Our results suggest that Ast could ameliorate the cognitive defects in APP/PS1 mice by activating the mTOR pathway. .. Astaxanthin (Ast) is an effective neuroprotective and antioxidant compound used to treat Alzheimer’s disease (AD); however, the underlying in vivomolecular mechanisms remain unknown.. In this study, we report that Ast can activate the mammalian target of rapamycin (mTOR) pathway in the 8-month-old APP/PS1 transgenic mouse model of AD.. Our results suggest that Ast could ameliorate the cognitive defects in APP/PS1 mice by activating the mTOR pathway.

    Article Title: Modulating Amyloid Pathology-Neural Hyperexcitability Crosstalk for Alzheimer's Disease Therapy.
    Article Snippet: Current therapies for Alzheimer’s disease (AD) primarily target amyloid-β (Aβ) pathology using monoclonal antibodies, yet their limited efficacy partly results from unintended exacerbation of neural hyperexcitability.. This highlights a critical but underappreciated link between Aβ clearance and neuronal network dysfunction.. Here, we designed R@AClipo, a nanotherapeutic platform that codelivers the TREM2 agonist peptide COG1410 and the glutamate modulator riluzole via Angiopep-2−modified liposomes capable of crossing the blood−brain barrier.

    Concentration Assay:

    Article Title: Astaxanthin Improved the Cognitive Deficits in APP/PS1 Transgenic Mice Via Selective Activation of mTOR.
    Article Snippet: .. Astaxanthin (Ast) is an effective neuroprotective and antioxidant compound used to treat Alzheimer’s disease (AD); however, the underlying in vivomolecular mechanisms remain unknown.. In this study, we report that Ast can activate the mammalian target of rapamycin (mTOR) pathway in the 8-month-old APP/PS1 transgenic mouse model of AD.. Our results suggest that Ast could ameliorate the cognitive defects in APP/PS1 mice by activating the mTOR pathway. .. Astaxanthin (Ast) is an effective neuroprotective and antioxidant compound used to treat Alzheimer’s disease (AD); however, the underlying in vivomolecular mechanisms remain unknown.. In this study, we report that Ast can activate the mammalian target of rapamycin (mTOR) pathway in the 8-month-old APP/PS1 transgenic mouse model of AD.. Our results suggest that Ast could ameliorate the cognitive defects in APP/PS1 mice by activating the mTOR pathway.

    Article Title: Modulating Amyloid Pathology-Neural Hyperexcitability Crosstalk for Alzheimer's Disease Therapy.
    Article Snippet: Current therapies for Alzheimer’s disease (AD) primarily target amyloid-β (Aβ) pathology using monoclonal antibodies, yet their limited efficacy partly results from unintended exacerbation of neural hyperexcitability.. This highlights a critical but underappreciated link between Aβ clearance and neuronal network dysfunction.. Here, we designed R@AClipo, a nanotherapeutic platform that codelivers the TREM2 agonist peptide COG1410 and the glutamate modulator riluzole via Angiopep-2−modified liposomes capable of crossing the blood−brain barrier.



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    Neuronal ADRA1 knockdown alleviates tauopathy and neuronal damage in 3xTg-AD mice. A Western blot analysis was conducted to assess the expression levels of p-Taus396, p-Tau202/205, p-Tau231 and Tau5 in the hippocampus tissue of the four group mice ( n = 6). Quantification analysis of p-Taus396 ( B ), p-Tau202/205 ( C ), p-Tau231 ( D ) and Tau5 ( E ) protein expression. F Western blot analysis of hippocampal APP and Aβ expression across groups ( n = 6). Quantification analysis of APP ( G ) and Aβ ( H ) protein expression. ELISA measurement of Aβ40 ( I ) and <t>Aβ42</t> ( J ) protein levels ( n = 4). K Representative images Golgi-Cox-stained hippocampal neurons. L Sholl analysis of dendritic complexity ( n = 5 neurons from three mice per group). M Representative images of Golgi-stained dendritic spines in hippocampal regions. N Quantitative analysis of dendritic spine density ( n = 12 neurons from three mice per group). O Western blot analysis of hippocampal PSD95 and Snap25 expression across groups ( n = 6). Quantification analysis of PSD95 ( P ) and Snap25 ( Q ) protein expression. Data are expressed as mean ± SEM, ** p < 0.01, *** p < 0.001, **** p < 0.0001
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    sensolyte anti-human aβ42 quantitative elisa colorimetric kit  (AnaSpec)
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    Amytrapper Catheter Capture <t>Aβ42</t> From Whole Blood in vivo in AD Rats. (A) Aβ42 From AD Rat Whole Blood Bound to Amytrapper Coated and Control Uncoated (Mock) Catheters at the End of the Treatment. After Treatment, Amytrapper Catheters and Mock Catheters Were Used for the Measurement of Catheter-Bound Aβ Through Designed Immunosorbent Assay. The Experiment Aimed to Determine the Effectiveness of Amytrapper-Coated Catheters in Capturing Aβ42 From the Bloodstream. Statistically Significant Difference Between the Mock Catheter (n = 20 Assay) and Amytrapper Catheter Treatment Groups (n = 41 Assay) is Expressed as *** P < 0.001, Cohen’s d = 3.496416, Utilizing Unpaired T-test. (B) Plasma Aβ42 From Rats before and after Catheter Treatments as Measured by <t>Sensolyte®</t> Quantitative <t>ELISA</t> kit. Plasma Aβ42 Levels before Mock Catheter (n = 7) or Amytrapper Catheter Treatment (n = 16) are Displayed as Blue Columns. Plasma Aβ42 Levels after third Mock Catheter (n = 6) or Amytrapper Catheter Treatment (n = 14) are Displayed as Yellow Columns. Plasma Aβ42 Levels after sixth Mock Catheter (n = 5) or Amytrapper Catheter Treatment (n = 6) are Displayed as Orange Columns. Statistically Significant Difference is Arrived by Comparing the Same Treatment (third Treatment and sixth Treatment) Between Mock Catheter Groups and Amytrapper Catheter Groups Using the Unpaired T-test. Statistically Significant Difference Between the Mock and Amytrapper Catheter Treatment Groups is Expressed (* P < 0.05, ** P < 0.01 Utilizing Unpaired T-test)
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    Neuronal ADRA1 knockdown alleviates tauopathy and neuronal damage in 3xTg-AD mice. A Western blot analysis was conducted to assess the expression levels of p-Taus396, p-Tau202/205, p-Tau231 and Tau5 in the hippocampus tissue of the four group mice ( n = 6). Quantification analysis of p-Taus396 ( B ), p-Tau202/205 ( C ), p-Tau231 ( D ) and Tau5 ( E ) protein expression. F Western blot analysis of hippocampal APP and Aβ expression across groups ( n = 6). Quantification analysis of APP ( G ) and Aβ ( H ) protein expression. ELISA measurement of Aβ40 ( I ) and Aβ42 ( J ) protein levels ( n = 4). K Representative images Golgi-Cox-stained hippocampal neurons. L Sholl analysis of dendritic complexity ( n = 5 neurons from three mice per group). M Representative images of Golgi-stained dendritic spines in hippocampal regions. N Quantitative analysis of dendritic spine density ( n = 12 neurons from three mice per group). O Western blot analysis of hippocampal PSD95 and Snap25 expression across groups ( n = 6). Quantification analysis of PSD95 ( P ) and Snap25 ( Q ) protein expression. Data are expressed as mean ± SEM, ** p < 0.01, *** p < 0.001, **** p < 0.0001

    Journal: Journal of Neuroinflammation

    Article Title: Modulation of neuronal α1-adrenergic receptor reduces tauopathy and neuroinflammation by inhibiting the STING/NF-κB/NLRP3 signaling pathway in Alzheimer’s disease mice

    doi: 10.1186/s12974-025-03506-3

    Figure Lengend Snippet: Neuronal ADRA1 knockdown alleviates tauopathy and neuronal damage in 3xTg-AD mice. A Western blot analysis was conducted to assess the expression levels of p-Taus396, p-Tau202/205, p-Tau231 and Tau5 in the hippocampus tissue of the four group mice ( n = 6). Quantification analysis of p-Taus396 ( B ), p-Tau202/205 ( C ), p-Tau231 ( D ) and Tau5 ( E ) protein expression. F Western blot analysis of hippocampal APP and Aβ expression across groups ( n = 6). Quantification analysis of APP ( G ) and Aβ ( H ) protein expression. ELISA measurement of Aβ40 ( I ) and Aβ42 ( J ) protein levels ( n = 4). K Representative images Golgi-Cox-stained hippocampal neurons. L Sholl analysis of dendritic complexity ( n = 5 neurons from three mice per group). M Representative images of Golgi-stained dendritic spines in hippocampal regions. N Quantitative analysis of dendritic spine density ( n = 12 neurons from three mice per group). O Western blot analysis of hippocampal PSD95 and Snap25 expression across groups ( n = 6). Quantification analysis of PSD95 ( P ) and Snap25 ( Q ) protein expression. Data are expressed as mean ± SEM, ** p < 0.01, *** p < 0.001, **** p < 0.0001

    Article Snippet: Supernatants were collected from each experimental group and protein concentrations of IL-1β (E-EL-H0149 and E-EL-M0037, Elabscience), IL-6 (E-EL-H6156, Elabscience), IL-18 (E-EL-H0253 and E-EL-M0730, Elabscience), Aβ40 (E-EL-H0542, Elabscience) and Aβ42 (E-EL-H0543, Elabscience) were quantified using commercially available ELISA kits following the manufacturer's instructions.

    Techniques: Knockdown, Western Blot, Expressing, Enzyme-linked Immunosorbent Assay, Staining

    Amytrapper Catheter Capture Aβ42 From Whole Blood in vivo in AD Rats. (A) Aβ42 From AD Rat Whole Blood Bound to Amytrapper Coated and Control Uncoated (Mock) Catheters at the End of the Treatment. After Treatment, Amytrapper Catheters and Mock Catheters Were Used for the Measurement of Catheter-Bound Aβ Through Designed Immunosorbent Assay. The Experiment Aimed to Determine the Effectiveness of Amytrapper-Coated Catheters in Capturing Aβ42 From the Bloodstream. Statistically Significant Difference Between the Mock Catheter (n = 20 Assay) and Amytrapper Catheter Treatment Groups (n = 41 Assay) is Expressed as *** P < 0.001, Cohen’s d = 3.496416, Utilizing Unpaired T-test. (B) Plasma Aβ42 From Rats before and after Catheter Treatments as Measured by Sensolyte® Quantitative ELISA kit. Plasma Aβ42 Levels before Mock Catheter (n = 7) or Amytrapper Catheter Treatment (n = 16) are Displayed as Blue Columns. Plasma Aβ42 Levels after third Mock Catheter (n = 6) or Amytrapper Catheter Treatment (n = 14) are Displayed as Yellow Columns. Plasma Aβ42 Levels after sixth Mock Catheter (n = 5) or Amytrapper Catheter Treatment (n = 6) are Displayed as Orange Columns. Statistically Significant Difference is Arrived by Comparing the Same Treatment (third Treatment and sixth Treatment) Between Mock Catheter Groups and Amytrapper Catheter Groups Using the Unpaired T-test. Statistically Significant Difference Between the Mock and Amytrapper Catheter Treatment Groups is Expressed (* P < 0.05, ** P < 0.01 Utilizing Unpaired T-test)

    Journal: American Journal of Alzheimer's Disease and Other Dementias

    Article Title: Amytrapper Catheter: A Prototype Extracorporeal Device That Traps Blood Amyloid-β in a Rat Model of Alzheimer’s Disease

    doi: 10.1177/15333175251361265

    Figure Lengend Snippet: Amytrapper Catheter Capture Aβ42 From Whole Blood in vivo in AD Rats. (A) Aβ42 From AD Rat Whole Blood Bound to Amytrapper Coated and Control Uncoated (Mock) Catheters at the End of the Treatment. After Treatment, Amytrapper Catheters and Mock Catheters Were Used for the Measurement of Catheter-Bound Aβ Through Designed Immunosorbent Assay. The Experiment Aimed to Determine the Effectiveness of Amytrapper-Coated Catheters in Capturing Aβ42 From the Bloodstream. Statistically Significant Difference Between the Mock Catheter (n = 20 Assay) and Amytrapper Catheter Treatment Groups (n = 41 Assay) is Expressed as *** P < 0.001, Cohen’s d = 3.496416, Utilizing Unpaired T-test. (B) Plasma Aβ42 From Rats before and after Catheter Treatments as Measured by Sensolyte® Quantitative ELISA kit. Plasma Aβ42 Levels before Mock Catheter (n = 7) or Amytrapper Catheter Treatment (n = 16) are Displayed as Blue Columns. Plasma Aβ42 Levels after third Mock Catheter (n = 6) or Amytrapper Catheter Treatment (n = 14) are Displayed as Yellow Columns. Plasma Aβ42 Levels after sixth Mock Catheter (n = 5) or Amytrapper Catheter Treatment (n = 6) are Displayed as Orange Columns. Statistically Significant Difference is Arrived by Comparing the Same Treatment (third Treatment and sixth Treatment) Between Mock Catheter Groups and Amytrapper Catheter Groups Using the Unpaired T-test. Statistically Significant Difference Between the Mock and Amytrapper Catheter Treatment Groups is Expressed (* P < 0.05, ** P < 0.01 Utilizing Unpaired T-test)

    Article Snippet: SensoLyte anti-human Aβ42 quantitative ELISA colorimetric kit (Anaspec, Fremont, CA) was used to estimate the amount of Aβ42 in plasma and CSF in rats.

    Techniques: In Vivo, Control, Clinical Proteomics, Enzyme-linked Immunosorbent Assay

    Cerebrospinal Fluid Aβ42 Levels in Mock and Amytrapper Catheter-Treated AD Rats. CSF Aβ42 From Rats before and after Catheter Treatments was Measured Using the Sensolyte® Quantitative ELISA kit. Following Two Months of Treatment, Rats Treated With the Amytrapper Catheter (n = 6) Displayed Slightly Higher Levels of Aβ42 in the CSF Compared to the Mock Catheter (n = 5) as Control Group ( P > 0.05; n.s, Utilizing Unpaired T-test)

    Journal: American Journal of Alzheimer's Disease and Other Dementias

    Article Title: Amytrapper Catheter: A Prototype Extracorporeal Device That Traps Blood Amyloid-β in a Rat Model of Alzheimer’s Disease

    doi: 10.1177/15333175251361265

    Figure Lengend Snippet: Cerebrospinal Fluid Aβ42 Levels in Mock and Amytrapper Catheter-Treated AD Rats. CSF Aβ42 From Rats before and after Catheter Treatments was Measured Using the Sensolyte® Quantitative ELISA kit. Following Two Months of Treatment, Rats Treated With the Amytrapper Catheter (n = 6) Displayed Slightly Higher Levels of Aβ42 in the CSF Compared to the Mock Catheter (n = 5) as Control Group ( P > 0.05; n.s, Utilizing Unpaired T-test)

    Article Snippet: SensoLyte anti-human Aβ42 quantitative ELISA colorimetric kit (Anaspec, Fremont, CA) was used to estimate the amount of Aβ42 in plasma and CSF in rats.

    Techniques: Enzyme-linked Immunosorbent Assay, Control