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msd approach  (Meso Scale Diagnostics LLC)

 
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    Meso Scale Diagnostics LLC msd approach
    Impact of AL002c treatment on <t>total</t> <t>Aβ</t> load. (A) Quantification of methoxy-X04 + area coverage in the cortex (Ctx) and hippocampus (HC) of treated mice. Each CV-KO-5XFAD treatment group, n = 7; each R47H-KO-5XFAD treatment group, n = 6. (B) Volume of individual methoxy-X04 + Aβ plaques in the cortex of indicated treatment groups. The volume of ∼1,000 plaques per condition was determined by Imaris. (C–F) PBS-soluble and PBS-insoluble guanidine-soluble fractions of hippocampus were assessed for Aβ 1–40 (C and E) and Aβ 1–42 (D and F) by <t>MSD.</t> Values for PBS-soluble Aβ 1–40 were below the limit of detection in some samples. Each CV-KO-5XFAD treatment group, n = 7; each R47H-KO-5XFAD treatment group, n = 6. No differences were detected for Aβ 1–40 or Aβ 1–42 in PBS-insoluble guanidine-soluble fractions of cortices among treatment groups (not depicted). PBS-soluble fractions of cortices showed no detectable Aβ 1–40 or Aβ 1–42 by MSD . *, P < 0.05; **, P < 0.01 by two-way ANOVA. Data are presented as mean ± SEM.
    Msd Approach, supplied by Meso Scale Diagnostics LLC, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/msd+approach/pmc07478730-115-15-13?v=Meso+Scale+Diagnostics+LLC
    Average 90 stars, based on 1 article reviews
    msd approach - by Bioz Stars, 2026-07
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    1) Product Images from "Anti-human TREM2 induces microglia proliferation and reduces pathology in an Alzheimer’s disease model"

    Article Title: Anti-human TREM2 induces microglia proliferation and reduces pathology in an Alzheimer’s disease model

    Journal: The Journal of Experimental Medicine

    doi: 10.1084/jem.20200785

    Impact of AL002c treatment on total Aβ load. (A) Quantification of methoxy-X04 + area coverage in the cortex (Ctx) and hippocampus (HC) of treated mice. Each CV-KO-5XFAD treatment group, n = 7; each R47H-KO-5XFAD treatment group, n = 6. (B) Volume of individual methoxy-X04 + Aβ plaques in the cortex of indicated treatment groups. The volume of ∼1,000 plaques per condition was determined by Imaris. (C–F) PBS-soluble and PBS-insoluble guanidine-soluble fractions of hippocampus were assessed for Aβ 1–40 (C and E) and Aβ 1–42 (D and F) by MSD. Values for PBS-soluble Aβ 1–40 were below the limit of detection in some samples. Each CV-KO-5XFAD treatment group, n = 7; each R47H-KO-5XFAD treatment group, n = 6. No differences were detected for Aβ 1–40 or Aβ 1–42 in PBS-insoluble guanidine-soluble fractions of cortices among treatment groups (not depicted). PBS-soluble fractions of cortices showed no detectable Aβ 1–40 or Aβ 1–42 by MSD . *, P < 0.05; **, P < 0.01 by two-way ANOVA. Data are presented as mean ± SEM.
    Figure Legend Snippet: Impact of AL002c treatment on total Aβ load. (A) Quantification of methoxy-X04 + area coverage in the cortex (Ctx) and hippocampus (HC) of treated mice. Each CV-KO-5XFAD treatment group, n = 7; each R47H-KO-5XFAD treatment group, n = 6. (B) Volume of individual methoxy-X04 + Aβ plaques in the cortex of indicated treatment groups. The volume of ∼1,000 plaques per condition was determined by Imaris. (C–F) PBS-soluble and PBS-insoluble guanidine-soluble fractions of hippocampus were assessed for Aβ 1–40 (C and E) and Aβ 1–42 (D and F) by MSD. Values for PBS-soluble Aβ 1–40 were below the limit of detection in some samples. Each CV-KO-5XFAD treatment group, n = 7; each R47H-KO-5XFAD treatment group, n = 6. No differences were detected for Aβ 1–40 or Aβ 1–42 in PBS-insoluble guanidine-soluble fractions of cortices among treatment groups (not depicted). PBS-soluble fractions of cortices showed no detectable Aβ 1–40 or Aβ 1–42 by MSD . *, P < 0.05; **, P < 0.01 by two-way ANOVA. Data are presented as mean ± SEM.

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    Impact of AL002c treatment on <t>total</t> <t>Aβ</t> load. (A) Quantification of methoxy-X04 + area coverage in the cortex (Ctx) and hippocampus (HC) of treated mice. Each CV-KO-5XFAD treatment group, n = 7; each R47H-KO-5XFAD treatment group, n = 6. (B) Volume of individual methoxy-X04 + Aβ plaques in the cortex of indicated treatment groups. The volume of ∼1,000 plaques per condition was determined by Imaris. (C–F) PBS-soluble and PBS-insoluble guanidine-soluble fractions of hippocampus were assessed for Aβ 1–40 (C and E) and Aβ 1–42 (D and F) by <t>MSD.</t> Values for PBS-soluble Aβ 1–40 were below the limit of detection in some samples. Each CV-KO-5XFAD treatment group, n = 7; each R47H-KO-5XFAD treatment group, n = 6. No differences were detected for Aβ 1–40 or Aβ 1–42 in PBS-insoluble guanidine-soluble fractions of cortices among treatment groups (not depicted). PBS-soluble fractions of cortices showed no detectable Aβ 1–40 or Aβ 1–42 by MSD . *, P < 0.05; **, P < 0.01 by two-way ANOVA. Data are presented as mean ± SEM.
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    Image Search Results


    Impact of AL002c treatment on total Aβ load. (A) Quantification of methoxy-X04 + area coverage in the cortex (Ctx) and hippocampus (HC) of treated mice. Each CV-KO-5XFAD treatment group, n = 7; each R47H-KO-5XFAD treatment group, n = 6. (B) Volume of individual methoxy-X04 + Aβ plaques in the cortex of indicated treatment groups. The volume of ∼1,000 plaques per condition was determined by Imaris. (C–F) PBS-soluble and PBS-insoluble guanidine-soluble fractions of hippocampus were assessed for Aβ 1–40 (C and E) and Aβ 1–42 (D and F) by MSD. Values for PBS-soluble Aβ 1–40 were below the limit of detection in some samples. Each CV-KO-5XFAD treatment group, n = 7; each R47H-KO-5XFAD treatment group, n = 6. No differences were detected for Aβ 1–40 or Aβ 1–42 in PBS-insoluble guanidine-soluble fractions of cortices among treatment groups (not depicted). PBS-soluble fractions of cortices showed no detectable Aβ 1–40 or Aβ 1–42 by MSD . *, P < 0.05; **, P < 0.01 by two-way ANOVA. Data are presented as mean ± SEM.

    Journal: The Journal of Experimental Medicine

    Article Title: Anti-human TREM2 induces microglia proliferation and reduces pathology in an Alzheimer’s disease model

    doi: 10.1084/jem.20200785

    Figure Lengend Snippet: Impact of AL002c treatment on total Aβ load. (A) Quantification of methoxy-X04 + area coverage in the cortex (Ctx) and hippocampus (HC) of treated mice. Each CV-KO-5XFAD treatment group, n = 7; each R47H-KO-5XFAD treatment group, n = 6. (B) Volume of individual methoxy-X04 + Aβ plaques in the cortex of indicated treatment groups. The volume of ∼1,000 plaques per condition was determined by Imaris. (C–F) PBS-soluble and PBS-insoluble guanidine-soluble fractions of hippocampus were assessed for Aβ 1–40 (C and E) and Aβ 1–42 (D and F) by MSD. Values for PBS-soluble Aβ 1–40 were below the limit of detection in some samples. Each CV-KO-5XFAD treatment group, n = 7; each R47H-KO-5XFAD treatment group, n = 6. No differences were detected for Aβ 1–40 or Aβ 1–42 in PBS-insoluble guanidine-soluble fractions of cortices among treatment groups (not depicted). PBS-soluble fractions of cortices showed no detectable Aβ 1–40 or Aβ 1–42 by MSD . *, P < 0.05; **, P < 0.01 by two-way ANOVA. Data are presented as mean ± SEM.

    Article Snippet: Aβ 1–40 and Aβ 1–42 levels were measured in both fractions by the Meso Scale Discovery (MSD) approach.

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