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Covance 4g8 monoclonal antibody against aβ
Diagram summarizing experimental workflow. Autopsy brain tissue from 273 volunteers diagnosed with intermediate/high Alzheimer’s disease was selected from 3 Alzheimer’s Disease Research Centers. Frontal, parietal, and temporal lobe sections were immunostained for Aβ <t>(4G8</t> antibody) and digitized into high-resolution whole-slide images (WSIs). WSIs were preprocessed, tiled, and analyzed using a machine learning pipeline that classified Aβ deposits (cored plaque—red, diffuse plaque—purple, and cerebral amyloid angiopathy [CAA]—dark blue) and segmented gray/white matter denoted by different colors (yellow for white matter [WM], cyan for gray matter [GM]) on the heatmaps. Deposit counts and densities were computed using spatially aligned heatmaps, followed by quality control checks and statistical analysis comparing plaque burden across demographic and clinical groups. Figure created using BioRender.
4g8 Monoclonal Antibody Against Aβ, supplied by Covance, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Diagram summarizing experimental workflow. Autopsy brain tissue from 273 volunteers diagnosed with intermediate/high Alzheimer’s disease was selected from 3 Alzheimer’s Disease Research Centers. Frontal, parietal, and temporal lobe sections were immunostained for Aβ <t>(4G8</t> antibody) and digitized into high-resolution whole-slide images (WSIs). WSIs were preprocessed, tiled, and analyzed using a machine learning pipeline that classified Aβ deposits (cored plaque—red, diffuse plaque—purple, and cerebral amyloid angiopathy [CAA]—dark blue) and segmented gray/white matter denoted by different colors (yellow for white matter [WM], cyan for gray matter [GM]) on the heatmaps. Deposit counts and densities were computed using spatially aligned heatmaps, followed by quality control checks and statistical analysis comparing plaque burden across demographic and clinical groups. Figure created using BioRender.
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Covance anti aβ antibody 4g8
Eight 12-month-old APP/PS1 mice were treated intraperitoneally with P33 (200 µg/kg/day), while eleven age-matched APP/PS1 mice received PBS as vehicle control. Injections were administered three times per week for eight consecutive weeks. (A) Aβ1-42 levels quantified by ELISA in soluble hemibrain extracts. (B) Representative immunohistochemistry images showing <t>4G8-positive</t> amyloid plaques in the CTX (left) and HIP (right) of 14-month-old mice, illustrating reduced plaque burden following P33 treatment compared to PBS control. (C) Quantification of amyloid plaques in the CTX shown in B, including average plaque size (μm²), percentage of area occupied by plaques, and plaque density (plaques/mm²). (D) Quantification of HIP amyloid plaques shown in B using the same parameters: average plaque size, plaque area percentage, and plaque density. Each dot represents one animal; shape code indicates sex (square: male; circle: female). Asterisks indicate statistically significant differences (* p < 0.05, ** p < 0.01, Student’s t -test). Abbreviations in B: CTX = Neocortex, HIP = Hippocampus, CA1-3 = Cornus ammonis 1-3, DG = Dentate gyrus .
Anti Aβ Antibody 4g8, supplied by Covance, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Novus Biologicals a parp2 mouse novus biologicals
Eight 12-month-old APP/PS1 mice were treated intraperitoneally with P33 (200 µg/kg/day), while eleven age-matched APP/PS1 mice received PBS as vehicle control. Injections were administered three times per week for eight consecutive weeks. (A) Aβ1-42 levels quantified by ELISA in soluble hemibrain extracts. (B) Representative immunohistochemistry images showing <t>4G8-positive</t> amyloid plaques in the CTX (left) and HIP (right) of 14-month-old mice, illustrating reduced plaque burden following P33 treatment compared to PBS control. (C) Quantification of amyloid plaques in the CTX shown in B, including average plaque size (μm²), percentage of area occupied by plaques, and plaque density (plaques/mm²). (D) Quantification of HIP amyloid plaques shown in B using the same parameters: average plaque size, plaque area percentage, and plaque density. Each dot represents one animal; shape code indicates sex (square: male; circle: female). Asterisks indicate statistically significant differences (* p < 0.05, ** p < 0.01, Student’s t -test). Abbreviations in B: CTX = Neocortex, HIP = Hippocampus, CA1-3 = Cornus ammonis 1-3, DG = Dentate gyrus .
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Covance 4g8 antibody
Amyloid-β plaque burden in the cortex and hippocampus of 5xFAD mice after B16F0 melanoma cell inoculation. Coronal brain sections from 5xFAD mice injected with either solvent or B16F0 melanoma cells were detected with the <t>4G8</t> antibody or ThS to detect amyloid-β (Aβ) plaques. ( A – B ) Representative images of 4G8 immunoreactivity in coronal brain sections of 5xFAD/solvent ( A ) and 5xFAD/B16F0 ( B ) mice. ( C – D ) Quantification of Aβ plaque burden (% area) in the cortex ( C ) and hippocampus ( D ) by immunostaining. ( E , F ) Number ( E ) and average size ( F ) of amyloid plaques determined with ThS staining in the hippocampus and cortex of 5xFAD inoculated with B16F0 or saline. No significant differences in plaque burden were observed between solvent- and B16F0-injected 5xFAD mice in either region. Data are presented as mean ± SEM (5xFAD/Solvent, n = 6; 5xFAD/ B16F0, n = 7 for 4G8 and n = 5 for ThS). Analyzed using One-Way ANOVA Tukey post hoc test, exact p values. Individual data points show male (circles) and female (triangles) mice. All mice genotypified as WT had negative ThS and 4G8 (Supplementary Fig. 6). Statistical analysis was performed using the Mann–Whitney U test. ( C ) ( p = 0.7028), ( D ) ( p = 0.8048), ( E ) ( p = 0.5476), ( F ) ( p = 0.8413). Scale Bar = 100 μm. Cx= cortex, Hipp= hippocampus.
4g8 Antibody, supplied by Covance, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Covance unlabeled 4g8 capture antibody
Amyloid-β plaque burden in the cortex and hippocampus of 5xFAD mice after B16F0 melanoma cell inoculation. Coronal brain sections from 5xFAD mice injected with either solvent or B16F0 melanoma cells were detected with the <t>4G8</t> antibody or ThS to detect amyloid-β (Aβ) plaques. ( A – B ) Representative images of 4G8 immunoreactivity in coronal brain sections of 5xFAD/solvent ( A ) and 5xFAD/B16F0 ( B ) mice. ( C – D ) Quantification of Aβ plaque burden (% area) in the cortex ( C ) and hippocampus ( D ) by immunostaining. ( E , F ) Number ( E ) and average size ( F ) of amyloid plaques determined with ThS staining in the hippocampus and cortex of 5xFAD inoculated with B16F0 or saline. No significant differences in plaque burden were observed between solvent- and B16F0-injected 5xFAD mice in either region. Data are presented as mean ± SEM (5xFAD/Solvent, n = 6; 5xFAD/ B16F0, n = 7 for 4G8 and n = 5 for ThS). Analyzed using One-Way ANOVA Tukey post hoc test, exact p values. Individual data points show male (circles) and female (triangles) mice. All mice genotypified as WT had negative ThS and 4G8 (Supplementary Fig. 6). Statistical analysis was performed using the Mann–Whitney U test. ( C ) ( p = 0.7028), ( D ) ( p = 0.8048), ( E ) ( p = 0.5476), ( F ) ( p = 0.8413). Scale Bar = 100 μm. Cx= cortex, Hipp= hippocampus.
Unlabeled 4g8 Capture Antibody, supplied by Covance, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Diagram summarizing experimental workflow. Autopsy brain tissue from 273 volunteers diagnosed with intermediate/high Alzheimer’s disease was selected from 3 Alzheimer’s Disease Research Centers. Frontal, parietal, and temporal lobe sections were immunostained for Aβ (4G8 antibody) and digitized into high-resolution whole-slide images (WSIs). WSIs were preprocessed, tiled, and analyzed using a machine learning pipeline that classified Aβ deposits (cored plaque—red, diffuse plaque—purple, and cerebral amyloid angiopathy [CAA]—dark blue) and segmented gray/white matter denoted by different colors (yellow for white matter [WM], cyan for gray matter [GM]) on the heatmaps. Deposit counts and densities were computed using spatially aligned heatmaps, followed by quality control checks and statistical analysis comparing plaque burden across demographic and clinical groups. Figure created using BioRender.

Journal: Journal of Neuropathology and Experimental Neurology

Article Title: Clinical and pathologic correlations of machine learning quantification of Aβ deposits across 3 brain regions of decedents with Alzheimer disease

doi: 10.1093/jnen/nlaf152

Figure Lengend Snippet: Diagram summarizing experimental workflow. Autopsy brain tissue from 273 volunteers diagnosed with intermediate/high Alzheimer’s disease was selected from 3 Alzheimer’s Disease Research Centers. Frontal, parietal, and temporal lobe sections were immunostained for Aβ (4G8 antibody) and digitized into high-resolution whole-slide images (WSIs). WSIs were preprocessed, tiled, and analyzed using a machine learning pipeline that classified Aβ deposits (cored plaque—red, diffuse plaque—purple, and cerebral amyloid angiopathy [CAA]—dark blue) and segmented gray/white matter denoted by different colors (yellow for white matter [WM], cyan for gray matter [GM]) on the heatmaps. Deposit counts and densities were computed using spatially aligned heatmaps, followed by quality control checks and statistical analysis comparing plaque burden across demographic and clinical groups. Figure created using BioRender.

Article Snippet: The 4G8 monoclonal antibody against Aβ (1:1600; Covance Labs, Madison, WI, United States) was utilized to perform immunohistochemical staining.

Techniques: Control

Eight 12-month-old APP/PS1 mice were treated intraperitoneally with P33 (200 µg/kg/day), while eleven age-matched APP/PS1 mice received PBS as vehicle control. Injections were administered three times per week for eight consecutive weeks. (A) Aβ1-42 levels quantified by ELISA in soluble hemibrain extracts. (B) Representative immunohistochemistry images showing 4G8-positive amyloid plaques in the CTX (left) and HIP (right) of 14-month-old mice, illustrating reduced plaque burden following P33 treatment compared to PBS control. (C) Quantification of amyloid plaques in the CTX shown in B, including average plaque size (μm²), percentage of area occupied by plaques, and plaque density (plaques/mm²). (D) Quantification of HIP amyloid plaques shown in B using the same parameters: average plaque size, plaque area percentage, and plaque density. Each dot represents one animal; shape code indicates sex (square: male; circle: female). Asterisks indicate statistically significant differences (* p < 0.05, ** p < 0.01, Student’s t -test). Abbreviations in B: CTX = Neocortex, HIP = Hippocampus, CA1-3 = Cornus ammonis 1-3, DG = Dentate gyrus .

Journal: bioRxiv

Article Title: cis-γ-Amino-L-proline peptides as chemical probes of amyloidogenic processing in neurons and APP/PS1 mice

doi: 10.64898/2026.04.17.719160

Figure Lengend Snippet: Eight 12-month-old APP/PS1 mice were treated intraperitoneally with P33 (200 µg/kg/day), while eleven age-matched APP/PS1 mice received PBS as vehicle control. Injections were administered three times per week for eight consecutive weeks. (A) Aβ1-42 levels quantified by ELISA in soluble hemibrain extracts. (B) Representative immunohistochemistry images showing 4G8-positive amyloid plaques in the CTX (left) and HIP (right) of 14-month-old mice, illustrating reduced plaque burden following P33 treatment compared to PBS control. (C) Quantification of amyloid plaques in the CTX shown in B, including average plaque size (μm²), percentage of area occupied by plaques, and plaque density (plaques/mm²). (D) Quantification of HIP amyloid plaques shown in B using the same parameters: average plaque size, plaque area percentage, and plaque density. Each dot represents one animal; shape code indicates sex (square: male; circle: female). Asterisks indicate statistically significant differences (* p < 0.05, ** p < 0.01, Student’s t -test). Abbreviations in B: CTX = Neocortex, HIP = Hippocampus, CA1-3 = Cornus ammonis 1-3, DG = Dentate gyrus .

Article Snippet: Afterwards, sections were incubated for 16 h at 4°C with the anti-Aβ antibody 4G8 (1:500; Covance, Princeton, NJ, USA).

Techniques: Control, Enzyme-linked Immunosorbent Assay, Immunohistochemistry

Amyloid-β plaque burden in the cortex and hippocampus of 5xFAD mice after B16F0 melanoma cell inoculation. Coronal brain sections from 5xFAD mice injected with either solvent or B16F0 melanoma cells were detected with the 4G8 antibody or ThS to detect amyloid-β (Aβ) plaques. ( A – B ) Representative images of 4G8 immunoreactivity in coronal brain sections of 5xFAD/solvent ( A ) and 5xFAD/B16F0 ( B ) mice. ( C – D ) Quantification of Aβ plaque burden (% area) in the cortex ( C ) and hippocampus ( D ) by immunostaining. ( E , F ) Number ( E ) and average size ( F ) of amyloid plaques determined with ThS staining in the hippocampus and cortex of 5xFAD inoculated with B16F0 or saline. No significant differences in plaque burden were observed between solvent- and B16F0-injected 5xFAD mice in either region. Data are presented as mean ± SEM (5xFAD/Solvent, n = 6; 5xFAD/ B16F0, n = 7 for 4G8 and n = 5 for ThS). Analyzed using One-Way ANOVA Tukey post hoc test, exact p values. Individual data points show male (circles) and female (triangles) mice. All mice genotypified as WT had negative ThS and 4G8 (Supplementary Fig. 6). Statistical analysis was performed using the Mann–Whitney U test. ( C ) ( p = 0.7028), ( D ) ( p = 0.8048), ( E ) ( p = 0.5476), ( F ) ( p = 0.8413). Scale Bar = 100 μm. Cx= cortex, Hipp= hippocampus.

Journal: Scientific Reports

Article Title: Melanoma cell inoculation improves cognitive impairment in the 5xFAD mouse model of Alzheimer’s disease

doi: 10.1038/s41598-026-40699-w

Figure Lengend Snippet: Amyloid-β plaque burden in the cortex and hippocampus of 5xFAD mice after B16F0 melanoma cell inoculation. Coronal brain sections from 5xFAD mice injected with either solvent or B16F0 melanoma cells were detected with the 4G8 antibody or ThS to detect amyloid-β (Aβ) plaques. ( A – B ) Representative images of 4G8 immunoreactivity in coronal brain sections of 5xFAD/solvent ( A ) and 5xFAD/B16F0 ( B ) mice. ( C – D ) Quantification of Aβ plaque burden (% area) in the cortex ( C ) and hippocampus ( D ) by immunostaining. ( E , F ) Number ( E ) and average size ( F ) of amyloid plaques determined with ThS staining in the hippocampus and cortex of 5xFAD inoculated with B16F0 or saline. No significant differences in plaque burden were observed between solvent- and B16F0-injected 5xFAD mice in either region. Data are presented as mean ± SEM (5xFAD/Solvent, n = 6; 5xFAD/ B16F0, n = 7 for 4G8 and n = 5 for ThS). Analyzed using One-Way ANOVA Tukey post hoc test, exact p values. Individual data points show male (circles) and female (triangles) mice. All mice genotypified as WT had negative ThS and 4G8 (Supplementary Fig. 6). Statistical analysis was performed using the Mann–Whitney U test. ( C ) ( p = 0.7028), ( D ) ( p = 0.8048), ( E ) ( p = 0.5476), ( F ) ( p = 0.8413). Scale Bar = 100 μm. Cx= cortex, Hipp= hippocampus.

Article Snippet: Sections were incubated overnight with a 1:1000 dilution of 4G8 antibody (Covance, NJ, USA) at room temperature, followed by a 2-hour incubation with goat anti-mouse HRP secondary antibody (1:1000, GE Healthcare Little Chalfont, UK).

Techniques: Injection, Solvent, Immunostaining, Staining, Saline, MANN-WHITNEY

Experimental design of the study. Experimental Set 1: WT and 5xFAD mice (5-months-old, both sexes) were subcutaneously inoculated with 4,000 B16F0 melanoma cells. Mice were monitored for 28 days to assess tumor growth and survival. At the end of the experiment, serum samples were collected for anti-B16F0 antibody detection, and spleens were harvested for flow cytometry analysis of immune cell populations. Experimental Set 2: WT and 5xFAD mice (5-months-old) were inoculated with either 4,000 B16F0 cells or solvent (saline) following the same procedure as in the first set. Starting on day 15, animals underwent behavioral testing, including Y-maze and Oasis maze tasks, following a habituation phase. On day 28, brain tissue was collected for immunofluorescence (GFAP and Iba1), amyloid staining (ThS and 4G8), and qPCR analysis of inflammatory markers ( Ifn -γ, Cxcl 10). Plasma samples were analyzed for cytokine levels by CBA. Common to Experimental Sets 1 and 2: tumor size was measured regularly throughout the 28-day period.

Journal: Scientific Reports

Article Title: Melanoma cell inoculation improves cognitive impairment in the 5xFAD mouse model of Alzheimer’s disease

doi: 10.1038/s41598-026-40699-w

Figure Lengend Snippet: Experimental design of the study. Experimental Set 1: WT and 5xFAD mice (5-months-old, both sexes) were subcutaneously inoculated with 4,000 B16F0 melanoma cells. Mice were monitored for 28 days to assess tumor growth and survival. At the end of the experiment, serum samples were collected for anti-B16F0 antibody detection, and spleens were harvested for flow cytometry analysis of immune cell populations. Experimental Set 2: WT and 5xFAD mice (5-months-old) were inoculated with either 4,000 B16F0 cells or solvent (saline) following the same procedure as in the first set. Starting on day 15, animals underwent behavioral testing, including Y-maze and Oasis maze tasks, following a habituation phase. On day 28, brain tissue was collected for immunofluorescence (GFAP and Iba1), amyloid staining (ThS and 4G8), and qPCR analysis of inflammatory markers ( Ifn -γ, Cxcl 10). Plasma samples were analyzed for cytokine levels by CBA. Common to Experimental Sets 1 and 2: tumor size was measured regularly throughout the 28-day period.

Article Snippet: Sections were incubated overnight with a 1:1000 dilution of 4G8 antibody (Covance, NJ, USA) at room temperature, followed by a 2-hour incubation with goat anti-mouse HRP secondary antibody (1:1000, GE Healthcare Little Chalfont, UK).

Techniques: Flow Cytometry, Solvent, Saline, Immunofluorescence, Staining, Clinical Proteomics