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aβ 1 42  (Cusabio)


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    Cusabio aβ 1 42
    OM-MSCs-Exo induced M2-polarized microglial cells through FGFR1 delivery, resulting in attenuated neuronal inflammation. <t>A</t> CCK8 assay in HT-22 and SH-SY5Y cells. B The apoptosis rate of HT-22 and SH-SY5Y cells was analyzed by flow cytometry. C IL-1β, TNF-α, and IL-6 levels of HT-22 and SH-SY5Y cells. The HT-22 cells in the Co-control group, <t>Co-Aβ</t> <t>1–42</t> group, Co-Aβ 1–42 + OM-MSCs-Exo group, Co-Aβ 1–42 + OM-MSCs-Exo oe−NC group, and Co-Aβ 1–42 + OM-MSCs-Exo oe−FGFR1 group were co-cultured with the corresponding BV2 cells for 24 h. The SH-SY5Y cells in the Co-control group, Co-Aβ 1–42 group, Co-Aβ 1–42 + OM-MSCs-Exo group, Co-Aβ 1–42 + OM-MSCs-Exo oe−NC group, and Co-Aβ 1–42 + OM-MSCs-Exo oe−FGFR1 group were co-cultured with the corresponding HMC3 cells for 24 h ( n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001. Normality was confirmed using the Shapiro–Wilk test. Thereafter, data were analyzed with a one-way ANOVA (followed by Tukey’s post hoc test) for multiple-group comparisons
    Aβ 1 42, supplied by Cusabio, used in various techniques. Bioz Stars score: 93/100, based on 24 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Olfactory Mucosa Mesenchymal Stem Cell–Derived Exosomes Enhance Microglia M2 Polarization via the FGFR1/PLCγ1 Axis to Alleviate Alzheimer’s Disease"

    Article Title: Olfactory Mucosa Mesenchymal Stem Cell–Derived Exosomes Enhance Microglia M2 Polarization via the FGFR1/PLCγ1 Axis to Alleviate Alzheimer’s Disease

    Journal: Molecular Neurobiology

    doi: 10.1007/s12035-026-05797-w

    OM-MSCs-Exo induced M2-polarized microglial cells through FGFR1 delivery, resulting in attenuated neuronal inflammation. A CCK8 assay in HT-22 and SH-SY5Y cells. B The apoptosis rate of HT-22 and SH-SY5Y cells was analyzed by flow cytometry. C IL-1β, TNF-α, and IL-6 levels of HT-22 and SH-SY5Y cells. The HT-22 cells in the Co-control group, Co-Aβ 1–42 group, Co-Aβ 1–42 + OM-MSCs-Exo group, Co-Aβ 1–42 + OM-MSCs-Exo oe−NC group, and Co-Aβ 1–42 + OM-MSCs-Exo oe−FGFR1 group were co-cultured with the corresponding BV2 cells for 24 h. The SH-SY5Y cells in the Co-control group, Co-Aβ 1–42 group, Co-Aβ 1–42 + OM-MSCs-Exo group, Co-Aβ 1–42 + OM-MSCs-Exo oe−NC group, and Co-Aβ 1–42 + OM-MSCs-Exo oe−FGFR1 group were co-cultured with the corresponding HMC3 cells for 24 h ( n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001. Normality was confirmed using the Shapiro–Wilk test. Thereafter, data were analyzed with a one-way ANOVA (followed by Tukey’s post hoc test) for multiple-group comparisons
    Figure Legend Snippet: OM-MSCs-Exo induced M2-polarized microglial cells through FGFR1 delivery, resulting in attenuated neuronal inflammation. A CCK8 assay in HT-22 and SH-SY5Y cells. B The apoptosis rate of HT-22 and SH-SY5Y cells was analyzed by flow cytometry. C IL-1β, TNF-α, and IL-6 levels of HT-22 and SH-SY5Y cells. The HT-22 cells in the Co-control group, Co-Aβ 1–42 group, Co-Aβ 1–42 + OM-MSCs-Exo group, Co-Aβ 1–42 + OM-MSCs-Exo oe−NC group, and Co-Aβ 1–42 + OM-MSCs-Exo oe−FGFR1 group were co-cultured with the corresponding BV2 cells for 24 h. The SH-SY5Y cells in the Co-control group, Co-Aβ 1–42 group, Co-Aβ 1–42 + OM-MSCs-Exo group, Co-Aβ 1–42 + OM-MSCs-Exo oe−NC group, and Co-Aβ 1–42 + OM-MSCs-Exo oe−FGFR1 group were co-cultured with the corresponding HMC3 cells for 24 h ( n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001. Normality was confirmed using the Shapiro–Wilk test. Thereafter, data were analyzed with a one-way ANOVA (followed by Tukey’s post hoc test) for multiple-group comparisons

    Techniques Used: CCK-8 Assay, Flow Cytometry, Control, Cell Culture

    OM-MSCs-Exo delivered FGFR1 to interact with PLCγ1 in microglia, suppressing the inflammatory response of co-cultured HT-22 and SH-SY5Y cells. A CCK8 assay in HT-22 and SH-SY5Y cells. B The apoptosis rate of neurons cells was analyzed by flow cytometry. C IL-1β, TNF-α, and IL-6 levels of HT-22 and SH-SY5Y cells. The HT-22 cells in the Co-Aβ 1–42 + OM-MSCs-Exo oe−NC group, Co-Aβ 1–42 + OM-MSCs-Exo oe−FGFR1 group, Co-Aβ 1–42 + OM-MSCs-Exo oe−FGFR1 + si-NC group, and Co-Aβ 1–42 + OM-MSCs-Exo oe−FGFR1 + si-PLCγ1 group were co-cultured with the corresponding BV2 cells for 24 h. The SH-SY5Y cells in the Co-Aβ 1–42 + OM-MSCs-Exo oe−NC group, Co-Aβ 1–42 + OM-MSCs-Exo oe−FGFR1 group, Co-Aβ 1–42 + OM-MSCs-Exo oe−FGFR1 + si-NC group, and Co-Aβ 1–42 + OM-MSCs-Exo oe−FGFR1 + si-PLCγ1 group were co-cultured with the corresponding HMC3 cells for 24 h ( n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001. Normality was confirmed using the Shapiro–Wilk test. Thereafter, data were analyzed with a one-way ANOVA (followed by Tukey’s post hoc test) for multiple-group comparisons
    Figure Legend Snippet: OM-MSCs-Exo delivered FGFR1 to interact with PLCγ1 in microglia, suppressing the inflammatory response of co-cultured HT-22 and SH-SY5Y cells. A CCK8 assay in HT-22 and SH-SY5Y cells. B The apoptosis rate of neurons cells was analyzed by flow cytometry. C IL-1β, TNF-α, and IL-6 levels of HT-22 and SH-SY5Y cells. The HT-22 cells in the Co-Aβ 1–42 + OM-MSCs-Exo oe−NC group, Co-Aβ 1–42 + OM-MSCs-Exo oe−FGFR1 group, Co-Aβ 1–42 + OM-MSCs-Exo oe−FGFR1 + si-NC group, and Co-Aβ 1–42 + OM-MSCs-Exo oe−FGFR1 + si-PLCγ1 group were co-cultured with the corresponding BV2 cells for 24 h. The SH-SY5Y cells in the Co-Aβ 1–42 + OM-MSCs-Exo oe−NC group, Co-Aβ 1–42 + OM-MSCs-Exo oe−FGFR1 group, Co-Aβ 1–42 + OM-MSCs-Exo oe−FGFR1 + si-NC group, and Co-Aβ 1–42 + OM-MSCs-Exo oe−FGFR1 + si-PLCγ1 group were co-cultured with the corresponding HMC3 cells for 24 h ( n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001. Normality was confirmed using the Shapiro–Wilk test. Thereafter, data were analyzed with a one-way ANOVA (followed by Tukey’s post hoc test) for multiple-group comparisons

    Techniques Used: Cell Culture, CCK-8 Assay, Flow Cytometry

    OM-MSCs-Exo alleviated cognitive impairment and neuroinflammation in AD mice through FGFR1. A Swimming distance, swimming time, number of platform arrivals, and latency to first entry ( n = 6). B The hippocampal tissues of mice were stained with HE. C Nissl staining was performed in the hippocampus of mice. D TUNEL assay. E Data plot of the TUNEL assay. F Levels of IL-1β, TNF-α, and IL-6 in mice hippocampus. G WB analysis of Aβ, p-Tau/Tau in mice hippocampus. H Aβ 1–42 levels were detected. I FGFR1 and PLCγ1 levels were measured. J Levels of p-NF-κB/NF-κB. K , L IF staining of CD86 and CD206 in mice hippocampus. M Levels of microglia M1 and M2 polarization–related factors in mice hippocampus ( n = 5). * p < 0.05, ** p < 0.01, *** p < 0.001. Normality was confirmed using the Shapiro–Wilk test. Thereafter, data were analyzed with a one-way ANOVA (followed by Tukey’s post hoc test) for multiple-group comparisons
    Figure Legend Snippet: OM-MSCs-Exo alleviated cognitive impairment and neuroinflammation in AD mice through FGFR1. A Swimming distance, swimming time, number of platform arrivals, and latency to first entry ( n = 6). B The hippocampal tissues of mice were stained with HE. C Nissl staining was performed in the hippocampus of mice. D TUNEL assay. E Data plot of the TUNEL assay. F Levels of IL-1β, TNF-α, and IL-6 in mice hippocampus. G WB analysis of Aβ, p-Tau/Tau in mice hippocampus. H Aβ 1–42 levels were detected. I FGFR1 and PLCγ1 levels were measured. J Levels of p-NF-κB/NF-κB. K , L IF staining of CD86 and CD206 in mice hippocampus. M Levels of microglia M1 and M2 polarization–related factors in mice hippocampus ( n = 5). * p < 0.05, ** p < 0.01, *** p < 0.001. Normality was confirmed using the Shapiro–Wilk test. Thereafter, data were analyzed with a one-way ANOVA (followed by Tukey’s post hoc test) for multiple-group comparisons

    Techniques Used: Staining, TUNEL Assay



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    Image Search Results


    OM-MSCs-Exo induced M2-polarized microglial cells through FGFR1 delivery, resulting in attenuated neuronal inflammation. A CCK8 assay in HT-22 and SH-SY5Y cells. B The apoptosis rate of HT-22 and SH-SY5Y cells was analyzed by flow cytometry. C IL-1β, TNF-α, and IL-6 levels of HT-22 and SH-SY5Y cells. The HT-22 cells in the Co-control group, Co-Aβ 1–42 group, Co-Aβ 1–42 + OM-MSCs-Exo group, Co-Aβ 1–42 + OM-MSCs-Exo oe−NC group, and Co-Aβ 1–42 + OM-MSCs-Exo oe−FGFR1 group were co-cultured with the corresponding BV2 cells for 24 h. The SH-SY5Y cells in the Co-control group, Co-Aβ 1–42 group, Co-Aβ 1–42 + OM-MSCs-Exo group, Co-Aβ 1–42 + OM-MSCs-Exo oe−NC group, and Co-Aβ 1–42 + OM-MSCs-Exo oe−FGFR1 group were co-cultured with the corresponding HMC3 cells for 24 h ( n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001. Normality was confirmed using the Shapiro–Wilk test. Thereafter, data were analyzed with a one-way ANOVA (followed by Tukey’s post hoc test) for multiple-group comparisons

    Journal: Molecular Neurobiology

    Article Title: Olfactory Mucosa Mesenchymal Stem Cell–Derived Exosomes Enhance Microglia M2 Polarization via the FGFR1/PLCγ1 Axis to Alleviate Alzheimer’s Disease

    doi: 10.1007/s12035-026-05797-w

    Figure Lengend Snippet: OM-MSCs-Exo induced M2-polarized microglial cells through FGFR1 delivery, resulting in attenuated neuronal inflammation. A CCK8 assay in HT-22 and SH-SY5Y cells. B The apoptosis rate of HT-22 and SH-SY5Y cells was analyzed by flow cytometry. C IL-1β, TNF-α, and IL-6 levels of HT-22 and SH-SY5Y cells. The HT-22 cells in the Co-control group, Co-Aβ 1–42 group, Co-Aβ 1–42 + OM-MSCs-Exo group, Co-Aβ 1–42 + OM-MSCs-Exo oe−NC group, and Co-Aβ 1–42 + OM-MSCs-Exo oe−FGFR1 group were co-cultured with the corresponding BV2 cells for 24 h. The SH-SY5Y cells in the Co-control group, Co-Aβ 1–42 group, Co-Aβ 1–42 + OM-MSCs-Exo group, Co-Aβ 1–42 + OM-MSCs-Exo oe−NC group, and Co-Aβ 1–42 + OM-MSCs-Exo oe−FGFR1 group were co-cultured with the corresponding HMC3 cells for 24 h ( n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001. Normality was confirmed using the Shapiro–Wilk test. Thereafter, data were analyzed with a one-way ANOVA (followed by Tukey’s post hoc test) for multiple-group comparisons

    Article Snippet: According to the instruction manuals of the mouse interleukin (IL)−1β (CSB-E08054m; Cusabio), tumor necrosis factor (TNF)-α (CSB-E04741m; Cusabio), IL-6 (CSB-E04639m; Cusabio), and Aβ 1–42 (CSB-E10787m; Cusabio) detection kits, the corresponding molecular levels in cells or tissues were measured.

    Techniques: CCK-8 Assay, Flow Cytometry, Control, Cell Culture

    OM-MSCs-Exo delivered FGFR1 to interact with PLCγ1 in microglia, suppressing the inflammatory response of co-cultured HT-22 and SH-SY5Y cells. A CCK8 assay in HT-22 and SH-SY5Y cells. B The apoptosis rate of neurons cells was analyzed by flow cytometry. C IL-1β, TNF-α, and IL-6 levels of HT-22 and SH-SY5Y cells. The HT-22 cells in the Co-Aβ 1–42 + OM-MSCs-Exo oe−NC group, Co-Aβ 1–42 + OM-MSCs-Exo oe−FGFR1 group, Co-Aβ 1–42 + OM-MSCs-Exo oe−FGFR1 + si-NC group, and Co-Aβ 1–42 + OM-MSCs-Exo oe−FGFR1 + si-PLCγ1 group were co-cultured with the corresponding BV2 cells for 24 h. The SH-SY5Y cells in the Co-Aβ 1–42 + OM-MSCs-Exo oe−NC group, Co-Aβ 1–42 + OM-MSCs-Exo oe−FGFR1 group, Co-Aβ 1–42 + OM-MSCs-Exo oe−FGFR1 + si-NC group, and Co-Aβ 1–42 + OM-MSCs-Exo oe−FGFR1 + si-PLCγ1 group were co-cultured with the corresponding HMC3 cells for 24 h ( n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001. Normality was confirmed using the Shapiro–Wilk test. Thereafter, data were analyzed with a one-way ANOVA (followed by Tukey’s post hoc test) for multiple-group comparisons

    Journal: Molecular Neurobiology

    Article Title: Olfactory Mucosa Mesenchymal Stem Cell–Derived Exosomes Enhance Microglia M2 Polarization via the FGFR1/PLCγ1 Axis to Alleviate Alzheimer’s Disease

    doi: 10.1007/s12035-026-05797-w

    Figure Lengend Snippet: OM-MSCs-Exo delivered FGFR1 to interact with PLCγ1 in microglia, suppressing the inflammatory response of co-cultured HT-22 and SH-SY5Y cells. A CCK8 assay in HT-22 and SH-SY5Y cells. B The apoptosis rate of neurons cells was analyzed by flow cytometry. C IL-1β, TNF-α, and IL-6 levels of HT-22 and SH-SY5Y cells. The HT-22 cells in the Co-Aβ 1–42 + OM-MSCs-Exo oe−NC group, Co-Aβ 1–42 + OM-MSCs-Exo oe−FGFR1 group, Co-Aβ 1–42 + OM-MSCs-Exo oe−FGFR1 + si-NC group, and Co-Aβ 1–42 + OM-MSCs-Exo oe−FGFR1 + si-PLCγ1 group were co-cultured with the corresponding BV2 cells for 24 h. The SH-SY5Y cells in the Co-Aβ 1–42 + OM-MSCs-Exo oe−NC group, Co-Aβ 1–42 + OM-MSCs-Exo oe−FGFR1 group, Co-Aβ 1–42 + OM-MSCs-Exo oe−FGFR1 + si-NC group, and Co-Aβ 1–42 + OM-MSCs-Exo oe−FGFR1 + si-PLCγ1 group were co-cultured with the corresponding HMC3 cells for 24 h ( n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001. Normality was confirmed using the Shapiro–Wilk test. Thereafter, data were analyzed with a one-way ANOVA (followed by Tukey’s post hoc test) for multiple-group comparisons

    Article Snippet: According to the instruction manuals of the mouse interleukin (IL)−1β (CSB-E08054m; Cusabio), tumor necrosis factor (TNF)-α (CSB-E04741m; Cusabio), IL-6 (CSB-E04639m; Cusabio), and Aβ 1–42 (CSB-E10787m; Cusabio) detection kits, the corresponding molecular levels in cells or tissues were measured.

    Techniques: Cell Culture, CCK-8 Assay, Flow Cytometry

    OM-MSCs-Exo alleviated cognitive impairment and neuroinflammation in AD mice through FGFR1. A Swimming distance, swimming time, number of platform arrivals, and latency to first entry ( n = 6). B The hippocampal tissues of mice were stained with HE. C Nissl staining was performed in the hippocampus of mice. D TUNEL assay. E Data plot of the TUNEL assay. F Levels of IL-1β, TNF-α, and IL-6 in mice hippocampus. G WB analysis of Aβ, p-Tau/Tau in mice hippocampus. H Aβ 1–42 levels were detected. I FGFR1 and PLCγ1 levels were measured. J Levels of p-NF-κB/NF-κB. K , L IF staining of CD86 and CD206 in mice hippocampus. M Levels of microglia M1 and M2 polarization–related factors in mice hippocampus ( n = 5). * p < 0.05, ** p < 0.01, *** p < 0.001. Normality was confirmed using the Shapiro–Wilk test. Thereafter, data were analyzed with a one-way ANOVA (followed by Tukey’s post hoc test) for multiple-group comparisons

    Journal: Molecular Neurobiology

    Article Title: Olfactory Mucosa Mesenchymal Stem Cell–Derived Exosomes Enhance Microglia M2 Polarization via the FGFR1/PLCγ1 Axis to Alleviate Alzheimer’s Disease

    doi: 10.1007/s12035-026-05797-w

    Figure Lengend Snippet: OM-MSCs-Exo alleviated cognitive impairment and neuroinflammation in AD mice through FGFR1. A Swimming distance, swimming time, number of platform arrivals, and latency to first entry ( n = 6). B The hippocampal tissues of mice were stained with HE. C Nissl staining was performed in the hippocampus of mice. D TUNEL assay. E Data plot of the TUNEL assay. F Levels of IL-1β, TNF-α, and IL-6 in mice hippocampus. G WB analysis of Aβ, p-Tau/Tau in mice hippocampus. H Aβ 1–42 levels were detected. I FGFR1 and PLCγ1 levels were measured. J Levels of p-NF-κB/NF-κB. K , L IF staining of CD86 and CD206 in mice hippocampus. M Levels of microglia M1 and M2 polarization–related factors in mice hippocampus ( n = 5). * p < 0.05, ** p < 0.01, *** p < 0.001. Normality was confirmed using the Shapiro–Wilk test. Thereafter, data were analyzed with a one-way ANOVA (followed by Tukey’s post hoc test) for multiple-group comparisons

    Article Snippet: According to the instruction manuals of the mouse interleukin (IL)−1β (CSB-E08054m; Cusabio), tumor necrosis factor (TNF)-α (CSB-E04741m; Cusabio), IL-6 (CSB-E04639m; Cusabio), and Aβ 1–42 (CSB-E10787m; Cusabio) detection kits, the corresponding molecular levels in cells or tissues were measured.

    Techniques: Staining, TUNEL Assay

    Therapeutic effects of GNNs on mouse hippocampal neuronal cells: ( A ) Electron microscopy results of Aβ 1–42 oligomers. ( B ) CCK8 detection results of mouse neuronal HT22 cells. ( C ) Detection of C6 cellular uptake rate (green fluorescence). Scale bar: 150μm. ( D ) Double staining results of mouse neuronal cells with Hoechst33342/PI (blue: Hoechst33342, red: PI). Scale bar: 150μm. ( E ) Quantification of Hoechst33342/PI fluorescence. ( F ) JC-1 fluorescence staining results of mouse neuronal cells (green: J-aggregate, red: J-monomer). Scale bar: 150 μm. ( G ) Quantification results of JC-1 fluorescence. ( H ) ROS fluorescence staining results of mouse neuronal HT22 cells (green: ROS signal). Scale bar: 150 μm. ( I ) Quantification results of ROS fluorescence. ( J ) IL-6. ( K ) IL-1β. ( L ) In vivo real-time imaging. *, p < 0.05 vs. Control; **, p < 0.01 vs. Control; #, p < 0.05 vs. Model; ##, p < 0.01 vs. Model.

    Journal: Pharmaceuticals

    Article Title: Self-Assembled Rg3/Naringenin Nanoparticles for Targeted Brain Delivery: A Promising Therapeutic Approach for Early Alzheimer’s Disease

    doi: 10.3390/ph19030367

    Figure Lengend Snippet: Therapeutic effects of GNNs on mouse hippocampal neuronal cells: ( A ) Electron microscopy results of Aβ 1–42 oligomers. ( B ) CCK8 detection results of mouse neuronal HT22 cells. ( C ) Detection of C6 cellular uptake rate (green fluorescence). Scale bar: 150μm. ( D ) Double staining results of mouse neuronal cells with Hoechst33342/PI (blue: Hoechst33342, red: PI). Scale bar: 150μm. ( E ) Quantification of Hoechst33342/PI fluorescence. ( F ) JC-1 fluorescence staining results of mouse neuronal cells (green: J-aggregate, red: J-monomer). Scale bar: 150 μm. ( G ) Quantification results of JC-1 fluorescence. ( H ) ROS fluorescence staining results of mouse neuronal HT22 cells (green: ROS signal). Scale bar: 150 μm. ( I ) Quantification results of ROS fluorescence. ( J ) IL-6. ( K ) IL-1β. ( L ) In vivo real-time imaging. *, p < 0.05 vs. Control; **, p < 0.01 vs. Control; #, p < 0.05 vs. Model; ##, p < 0.01 vs. Model.

    Article Snippet: Aβ 1–42 peptide was purchased from Macklin Biochemical Co., Ltd., Shanghai, China.

    Techniques: Electron Microscopy, Fluorescence, Double Staining, Staining, In Vivo, Imaging, Control

    GNNs improve neuronal apoptosis in the brains of AD mice: ( A ) HE staining images of CA1, CA2, and DG regions in mouse hippocampus. Scale bar: 150 μm. ( B ) Percentage of healthy cells. ( C ) Nissl staining images of CA1, CA2, and DG regions in mouse hippocampus. Scale bar: 150 μm. ( D ) Number of healthy Nissl bodies. ( E ) Aβ immunohistochemical staining images. Scale bar: 150 μm. ( F ) Quantitative analysis of Aβ 1–42 immunohistochemical staining. ( G ) Iba-1 immunohistochemical staining images. Scale bar: 150 μm. ( H ) Quantitative analysis of Iba-1 immunohistochemical staining. ( I ) Tau immunohistochemical staining images. Scale bar: 150 μm. ( J ) Quantitative analysis of Tau immunohistochemical staining. ( K ) GFAP immunohistochemical staining images. Scale bar: 150 μm. ( L ) Quantitative analysis of GFAP immunohistochemical staining. **, p < 0.01 vs. Control; ##, p < 0.01 vs. Model.

    Journal: Pharmaceuticals

    Article Title: Self-Assembled Rg3/Naringenin Nanoparticles for Targeted Brain Delivery: A Promising Therapeutic Approach for Early Alzheimer’s Disease

    doi: 10.3390/ph19030367

    Figure Lengend Snippet: GNNs improve neuronal apoptosis in the brains of AD mice: ( A ) HE staining images of CA1, CA2, and DG regions in mouse hippocampus. Scale bar: 150 μm. ( B ) Percentage of healthy cells. ( C ) Nissl staining images of CA1, CA2, and DG regions in mouse hippocampus. Scale bar: 150 μm. ( D ) Number of healthy Nissl bodies. ( E ) Aβ immunohistochemical staining images. Scale bar: 150 μm. ( F ) Quantitative analysis of Aβ 1–42 immunohistochemical staining. ( G ) Iba-1 immunohistochemical staining images. Scale bar: 150 μm. ( H ) Quantitative analysis of Iba-1 immunohistochemical staining. ( I ) Tau immunohistochemical staining images. Scale bar: 150 μm. ( J ) Quantitative analysis of Tau immunohistochemical staining. ( K ) GFAP immunohistochemical staining images. Scale bar: 150 μm. ( L ) Quantitative analysis of GFAP immunohistochemical staining. **, p < 0.01 vs. Control; ##, p < 0.01 vs. Model.

    Article Snippet: Aβ 1–42 peptide was purchased from Macklin Biochemical Co., Ltd., Shanghai, China.

    Techniques: Staining, Immunohistochemical staining, Control

    Integrative multi‐cell type analysis workflow identifies DISC1 as a convergent target of TSA in AD. Schematic representation of the multi‐pronged analytical framework used to identify and validate TSA as a therapeutic candidate for AD. The workflow began with cell‐type‐specific drug repurposing analysis of scRNA‐seq data from Grubman et al., <xref ref-type= 13 Mathys et al., 14 and Green et al. 15 datasets, resulting in the identification of TSA as a promising compound. We strategically investigated TSA's effects through two parallel cell type‐specific pathways: neurons and microglia. These cell types were specifically selected based on their known vulnerability in AD pathology and significant drug scores in our initial ASGARD analysis. For neurons, we applied DEGAS analysis to identify AD‐associated neuronal subpopulations, followed by differential expression analysis of TSA‐treated neurons in mice. Concurrently, we examined microglia, which showed high TSA drug scores in doublet interactions, and conducted differential expression analysis across microglial subtypes. Both analytical branches converged on DISC1 as a key upregulated gene, which was subsequently validated in human iPSC‐derived neuronal models through both phenotypic assays and transcriptomic analysis. This cell type‐specific approach enabled the identification of DISC1 as a potential mechanistic target underlying TSA's neuroprotective effect in AD. Created in BioRender. Peyton, M. (2025) https://biorender.com/73irecf . AD, Alzheimer's disease; ASGARD, A Single Cell Guided Pipeline to Aid Repurposing of Drugs; DEGAS, Diagnostic Evidence Gauge of Single cells; DISC1, Disrupted‐In‐Schizophrenia 1; iPSC, induced pluripotent stem cell; scRNA‐seq, single‐cell RNA sequencing; TSA, trichostatin‐A. " width="100%" height="100%">

    Journal: Alzheimer's & Dementia

    Article Title: Single‐cell analysis reveals neuroprotective histone deacetylase inhibitor pathways

    doi: 10.1002/alz.71108

    Figure Lengend Snippet: Integrative multi‐cell type analysis workflow identifies DISC1 as a convergent target of TSA in AD. Schematic representation of the multi‐pronged analytical framework used to identify and validate TSA as a therapeutic candidate for AD. The workflow began with cell‐type‐specific drug repurposing analysis of scRNA‐seq data from Grubman et al., 13 Mathys et al., 14 and Green et al. 15 datasets, resulting in the identification of TSA as a promising compound. We strategically investigated TSA's effects through two parallel cell type‐specific pathways: neurons and microglia. These cell types were specifically selected based on their known vulnerability in AD pathology and significant drug scores in our initial ASGARD analysis. For neurons, we applied DEGAS analysis to identify AD‐associated neuronal subpopulations, followed by differential expression analysis of TSA‐treated neurons in mice. Concurrently, we examined microglia, which showed high TSA drug scores in doublet interactions, and conducted differential expression analysis across microglial subtypes. Both analytical branches converged on DISC1 as a key upregulated gene, which was subsequently validated in human iPSC‐derived neuronal models through both phenotypic assays and transcriptomic analysis. This cell type‐specific approach enabled the identification of DISC1 as a potential mechanistic target underlying TSA's neuroprotective effect in AD. Created in BioRender. Peyton, M. (2025) https://biorender.com/73irecf . AD, Alzheimer's disease; ASGARD, A Single Cell Guided Pipeline to Aid Repurposing of Drugs; DEGAS, Diagnostic Evidence Gauge of Single cells; DISC1, Disrupted‐In‐Schizophrenia 1; iPSC, induced pluripotent stem cell; scRNA‐seq, single‐cell RNA sequencing; TSA, trichostatin‐A.

    Article Snippet: For experimental treatments, neurons were cultured until in vitro day (DIV) 4, at which point they were treated with various concentrations of TSA (TSA, Sigma–Aldrich, cat. #: T1952) and Aβ oligomers (StressMarq, cat. #: SPR‐488).

    Techniques: Quantitative Proteomics, Derivative Assay, Diagnostic Assay, RNA Sequencing

    Single‐cell analysis identifies TSA as top drug repurposing candidate across cortical brain regions. (A) UMAP projections of all cells from six control and six AD samples in the Grubman et al. <xref ref-type= 13 entorhinal cortex dataset, with clusters representing cell‐type‐specific groupings. (B) Pathway enrichment analysis highlighting key signaling pathways significantly enriched within each cell type cluster in the Grubman dataset, with significance represented as ‐log10(FDR). (C) Drug Score analysis for AD samples in the Grubman dataset, displaying compounds with FDR < 0.1 and Drug Score ranking within the 90th percentile. TSA (trichostatin‐A) emerges among the top‐ranked candidates. (D) UMAP visualizations of all cells from 24 control and 24 AD samples in the Mathys et al. 14 prefrontal cortex dataset, with distinct clusters representing cell types. (E) Pathway enrichment analysis for the Mathys dataset showing key signaling pathways significantly enriched within each cell type cluster, with significance represented as ‐log10(FDR). (F) Drug Score analysis for AD samples in the Mathys dataset, displaying compounds with FDR < 0.1 and Drug Score values within the 90th percentile. (G) UMAP projections from the Green et al. 15 aged prefrontal cortex dataset showing cell‐type‐specific clustering across AD and control samples. (H) Pathway enrichment analysis for the Green dataset, highlighting significantly enriched signaling pathways across cell types, with significance represented as ‐log10(FDR). (I) Drug Score analysis for the Green dataset showing top‐ranked therapeutic candidates with FDR < 0.1 and Drug Scores within the 90th percentile. Cell types: Ast, astrocytes; CUX2+, CUX2‐positive excitatory neurons; CUX2‐, CUX2‐negative excitatory neurons; Dou, doublets; End, endothelial cells; Ex, excitatory neurons; In, inhibitory neurons; Inh, inhibitory neurons; Mic, microglia; Neu, neurons; Oli, oligodendrocytes; Opc, oligodendrocyte progenitor cells; Per, pericytes; unID, unidentified cells. AD, Alzheimer's disease; FDR, false discovery rate; TSA, trichostatin‐A; UMAP, Uniform Manifold Approximation and Projection. " width="100%" height="100%">

    Journal: Alzheimer's & Dementia

    Article Title: Single‐cell analysis reveals neuroprotective histone deacetylase inhibitor pathways

    doi: 10.1002/alz.71108

    Figure Lengend Snippet: Single‐cell analysis identifies TSA as top drug repurposing candidate across cortical brain regions. (A) UMAP projections of all cells from six control and six AD samples in the Grubman et al. 13 entorhinal cortex dataset, with clusters representing cell‐type‐specific groupings. (B) Pathway enrichment analysis highlighting key signaling pathways significantly enriched within each cell type cluster in the Grubman dataset, with significance represented as ‐log10(FDR). (C) Drug Score analysis for AD samples in the Grubman dataset, displaying compounds with FDR < 0.1 and Drug Score ranking within the 90th percentile. TSA (trichostatin‐A) emerges among the top‐ranked candidates. (D) UMAP visualizations of all cells from 24 control and 24 AD samples in the Mathys et al. 14 prefrontal cortex dataset, with distinct clusters representing cell types. (E) Pathway enrichment analysis for the Mathys dataset showing key signaling pathways significantly enriched within each cell type cluster, with significance represented as ‐log10(FDR). (F) Drug Score analysis for AD samples in the Mathys dataset, displaying compounds with FDR < 0.1 and Drug Score values within the 90th percentile. (G) UMAP projections from the Green et al. 15 aged prefrontal cortex dataset showing cell‐type‐specific clustering across AD and control samples. (H) Pathway enrichment analysis for the Green dataset, highlighting significantly enriched signaling pathways across cell types, with significance represented as ‐log10(FDR). (I) Drug Score analysis for the Green dataset showing top‐ranked therapeutic candidates with FDR < 0.1 and Drug Scores within the 90th percentile. Cell types: Ast, astrocytes; CUX2+, CUX2‐positive excitatory neurons; CUX2‐, CUX2‐negative excitatory neurons; Dou, doublets; End, endothelial cells; Ex, excitatory neurons; In, inhibitory neurons; Inh, inhibitory neurons; Mic, microglia; Neu, neurons; Oli, oligodendrocytes; Opc, oligodendrocyte progenitor cells; Per, pericytes; unID, unidentified cells. AD, Alzheimer's disease; FDR, false discovery rate; TSA, trichostatin‐A; UMAP, Uniform Manifold Approximation and Projection.

    Article Snippet: For experimental treatments, neurons were cultured until in vitro day (DIV) 4, at which point they were treated with various concentrations of TSA (TSA, Sigma–Aldrich, cat. #: T1952) and Aβ oligomers (StressMarq, cat. #: SPR‐488).

    Techniques: Single-cell Analysis, Control, Protein-Protein interactions

    Doublet cell analysis reveals cellular interaction patterns and drug targeting opportunities in AD. (A) UMAP projections of all cells from six control and six AD samples in the Grubman et al. <xref ref-type= 13 dataset, showing cell‐type‐specific clusters with doublets re‐annotated into their most likely two contributing cell types (e.g., ast‐mic for astrocyte–microglia doublets). (B) Bar chart displaying the counts of identified cell types, including doublets without splitting into their component cell types. (C) Pie chart illustrating the distribution of identified doublet cell types, providing an overview of the most common cellular interactions observed in the dataset. (D) Pathway enrichment analysis for re‐annotated cell type clusters, highlighting key signaling pathways with significant enrichment, represented as ‐log10(FDR). (E) Drug Score analysis for AD samples, highlighting compounds with FDR < 0.1 and Drug Scores within the 90th percentile. TSA shows particularly strong enrichment in doublet populations involving microglia. Cell types: Ast, astrocytes; Dou, doublets; End, endothelial cells; Mic, microglia; Neu, neurons; Oli, oligodendrocytes; Opc, oligodendrocyte progenitor cells; unID, unidentified cells. AD, Alzheimer's disease; FDR, false discovery rate; UMAP, Uniform Manifold Approximation and Projection. " width="100%" height="100%">

    Journal: Alzheimer's & Dementia

    Article Title: Single‐cell analysis reveals neuroprotective histone deacetylase inhibitor pathways

    doi: 10.1002/alz.71108

    Figure Lengend Snippet: Doublet cell analysis reveals cellular interaction patterns and drug targeting opportunities in AD. (A) UMAP projections of all cells from six control and six AD samples in the Grubman et al. 13 dataset, showing cell‐type‐specific clusters with doublets re‐annotated into their most likely two contributing cell types (e.g., ast‐mic for astrocyte–microglia doublets). (B) Bar chart displaying the counts of identified cell types, including doublets without splitting into their component cell types. (C) Pie chart illustrating the distribution of identified doublet cell types, providing an overview of the most common cellular interactions observed in the dataset. (D) Pathway enrichment analysis for re‐annotated cell type clusters, highlighting key signaling pathways with significant enrichment, represented as ‐log10(FDR). (E) Drug Score analysis for AD samples, highlighting compounds with FDR < 0.1 and Drug Scores within the 90th percentile. TSA shows particularly strong enrichment in doublet populations involving microglia. Cell types: Ast, astrocytes; Dou, doublets; End, endothelial cells; Mic, microglia; Neu, neurons; Oli, oligodendrocytes; Opc, oligodendrocyte progenitor cells; unID, unidentified cells. AD, Alzheimer's disease; FDR, false discovery rate; UMAP, Uniform Manifold Approximation and Projection.

    Article Snippet: For experimental treatments, neurons were cultured until in vitro day (DIV) 4, at which point they were treated with various concentrations of TSA (TSA, Sigma–Aldrich, cat. #: T1952) and Aβ oligomers (StressMarq, cat. #: SPR‐488).

    Techniques: Cell Analysis, Control, Protein-Protein interactions

    TSA modulates synaptic and developmental gene programs and prevents Aβ‐induced neurotoxicity in human iPSC‐derived cortical neurons. (A) Volcano plot of DEGs in TSA‐treated mouse hippocampal neurons versus control. Blue points represent significantly downregulated genes, while red points represent significantly upregulated genes (adjusted p ‐value < 0.05). (B) GO Biological Process enrichment analysis for genes with positive log2 fold change (upregulated by TSA treatment). (C) GO Biological Process enrichment analysis for genes with negative log2 fold change (downregulated by TSA treatment). (D) Venn diagram showing overlapping upregulated genes across three independent analyses: TSA‐treated mouse hippocampal neurons (red, 5015 unique genes), microglial subtypes from the Lee et al. human dataset (blue, 419 unique genes), and AD‐associated neurons identified via DEGAS cell prioritization analysis (green, 142 unique genes). The diagram reveals 104 genes shared between the TSA and Lee datasets, 54 genes shared between the TSA and DEGAS, 4 genes shared between Lee and DEGAS, and critically, 1 gene (DISC1) upregulated across all three experimental contexts, identifying it as a convergent therapeutic target. (E) MTS cell viability assay results in human iPSC‐derived cortical neurons. Left panel: Dose‐response curve showing Aβ oligomer‐induced toxicity at concentrations of 0.2, 1, and 5 µM compared to control. Right panel: TSA neuroprotection against 5 µM Aβ oligomers, with neurons pre‐treated with varying TSA concentrations (0.066, 0.2, 0.33) showing dose‐dependent rescue of cell viability. Statistical significance: ns (not significant), ** p < 0.01, *** p < 0.001, **** p < 0.0001. (F) Quantification of synaptic cluster density (number of clusters per 20 µm dendrite) across treatment conditions. NT neurons show baseline synaptic density (gray), 5 µM) cause significant synaptic loss (red), and co‐treatment with 0.2 µM TSA (Aβo + TSA, green) significantly rescues synaptic density, demonstrating TSA's protective effect on synaptic integrity. Each dot represents an individual measurement. Statistical significance: ns (not significant), **** p < 0.0001. (G) Representative confocal immunofluorescence images of synapses in human iPSC‐derived cortical neurons. Neurons were immunostained for the postsynaptic marker PSD95 (red, left column) and presynaptic marker Syn1 (green, middle column), with colocalization (yellow, right column) indicating functional synapses. Rows show: NT controls (top), 5 µM Aβo treatment (middle), and combined treatment with Aβo plus 0.2 µM TSA (Aβo+TSA, bottom). TSA treatment preserves synaptic density and colocalization despite Aβ exposure. Scale bar = 2 µm. Aβ, β‐amyloid; Aβo, Aβ oligomers; AD, Alzheimer's disease; DEG, differentially expressed genes; DEGAS, Diagnostic Evidence Gauge of Single cells; GO, gene ontology; iPSC, induced pluripotent stem cell; NT, non‐treated; TSA, trichostatin‐A.

    Journal: Alzheimer's & Dementia

    Article Title: Single‐cell analysis reveals neuroprotective histone deacetylase inhibitor pathways

    doi: 10.1002/alz.71108

    Figure Lengend Snippet: TSA modulates synaptic and developmental gene programs and prevents Aβ‐induced neurotoxicity in human iPSC‐derived cortical neurons. (A) Volcano plot of DEGs in TSA‐treated mouse hippocampal neurons versus control. Blue points represent significantly downregulated genes, while red points represent significantly upregulated genes (adjusted p ‐value < 0.05). (B) GO Biological Process enrichment analysis for genes with positive log2 fold change (upregulated by TSA treatment). (C) GO Biological Process enrichment analysis for genes with negative log2 fold change (downregulated by TSA treatment). (D) Venn diagram showing overlapping upregulated genes across three independent analyses: TSA‐treated mouse hippocampal neurons (red, 5015 unique genes), microglial subtypes from the Lee et al. human dataset (blue, 419 unique genes), and AD‐associated neurons identified via DEGAS cell prioritization analysis (green, 142 unique genes). The diagram reveals 104 genes shared between the TSA and Lee datasets, 54 genes shared between the TSA and DEGAS, 4 genes shared between Lee and DEGAS, and critically, 1 gene (DISC1) upregulated across all three experimental contexts, identifying it as a convergent therapeutic target. (E) MTS cell viability assay results in human iPSC‐derived cortical neurons. Left panel: Dose‐response curve showing Aβ oligomer‐induced toxicity at concentrations of 0.2, 1, and 5 µM compared to control. Right panel: TSA neuroprotection against 5 µM Aβ oligomers, with neurons pre‐treated with varying TSA concentrations (0.066, 0.2, 0.33) showing dose‐dependent rescue of cell viability. Statistical significance: ns (not significant), ** p < 0.01, *** p < 0.001, **** p < 0.0001. (F) Quantification of synaptic cluster density (number of clusters per 20 µm dendrite) across treatment conditions. NT neurons show baseline synaptic density (gray), 5 µM) cause significant synaptic loss (red), and co‐treatment with 0.2 µM TSA (Aβo + TSA, green) significantly rescues synaptic density, demonstrating TSA's protective effect on synaptic integrity. Each dot represents an individual measurement. Statistical significance: ns (not significant), **** p < 0.0001. (G) Representative confocal immunofluorescence images of synapses in human iPSC‐derived cortical neurons. Neurons were immunostained for the postsynaptic marker PSD95 (red, left column) and presynaptic marker Syn1 (green, middle column), with colocalization (yellow, right column) indicating functional synapses. Rows show: NT controls (top), 5 µM Aβo treatment (middle), and combined treatment with Aβo plus 0.2 µM TSA (Aβo+TSA, bottom). TSA treatment preserves synaptic density and colocalization despite Aβ exposure. Scale bar = 2 µm. Aβ, β‐amyloid; Aβo, Aβ oligomers; AD, Alzheimer's disease; DEG, differentially expressed genes; DEGAS, Diagnostic Evidence Gauge of Single cells; GO, gene ontology; iPSC, induced pluripotent stem cell; NT, non‐treated; TSA, trichostatin‐A.

    Article Snippet: For experimental treatments, neurons were cultured until in vitro day (DIV) 4, at which point they were treated with various concentrations of TSA (TSA, Sigma–Aldrich, cat. #: T1952) and Aβ oligomers (StressMarq, cat. #: SPR‐488).

    Techniques: Derivative Assay, Control, Viability Assay, Immunofluorescence, Marker, Functional Assay, Diagnostic Assay

    Transcriptomic analysis of TSA effects on iPSC‐derived cortical neurons reveals distinct gene expression patterns . (A) Volcano plot displaying DEGs between control and TSA‐treated human iPSC‐derived cortical neurons. Significantly upregulated genes are shown in red and downregulated genes in blue (adjusted p ‐value < 0.05, |log 2 FC| > 0.58). (B) Box plots showing DISC1 expression levels (normalized log2CPM) across four treatment conditions: Control, Amyloid_beta (Aβ alone), TSA (TSA alone), and Combined (TSA + Aβ). Statistical comparisons are indicated with brackets and significance levels. (C) GO Biological Process enrichment analysis for genes upregulated by TSA treatment. Dot size represents gene count, and color indicates ‐log 10 (FDR). (D) GO Biological Process enrichment analysis for genes downregulated by TSA treatment. (E) GO Molecular Function enrichment for genes upregulated by TSA treatment. (F) GO Molecular Function enrichment for genes downregulated by TSA treatment. (G) Heatmap showing expression patterns of top differentially expressed genes across all samples. Samples are grouped by treatment condition (Control, Amyloid_beta, TSA, Combined) with color‐coded bars at the top. Gene expression is displayed as normalized z ‐scores, with red indicating high expression and blue indicating low expression. Aβ, β‐amyloid; DEG, differentially expressed genes; DISC1, Disrupted‐In‐Schizophrenia 1; FDR, false discovery rate; GO, gene ontology; iPSC, induced pluripotent stem cell; TSA, trichostatin‐A.

    Journal: Alzheimer's & Dementia

    Article Title: Single‐cell analysis reveals neuroprotective histone deacetylase inhibitor pathways

    doi: 10.1002/alz.71108

    Figure Lengend Snippet: Transcriptomic analysis of TSA effects on iPSC‐derived cortical neurons reveals distinct gene expression patterns . (A) Volcano plot displaying DEGs between control and TSA‐treated human iPSC‐derived cortical neurons. Significantly upregulated genes are shown in red and downregulated genes in blue (adjusted p ‐value < 0.05, |log 2 FC| > 0.58). (B) Box plots showing DISC1 expression levels (normalized log2CPM) across four treatment conditions: Control, Amyloid_beta (Aβ alone), TSA (TSA alone), and Combined (TSA + Aβ). Statistical comparisons are indicated with brackets and significance levels. (C) GO Biological Process enrichment analysis for genes upregulated by TSA treatment. Dot size represents gene count, and color indicates ‐log 10 (FDR). (D) GO Biological Process enrichment analysis for genes downregulated by TSA treatment. (E) GO Molecular Function enrichment for genes upregulated by TSA treatment. (F) GO Molecular Function enrichment for genes downregulated by TSA treatment. (G) Heatmap showing expression patterns of top differentially expressed genes across all samples. Samples are grouped by treatment condition (Control, Amyloid_beta, TSA, Combined) with color‐coded bars at the top. Gene expression is displayed as normalized z ‐scores, with red indicating high expression and blue indicating low expression. Aβ, β‐amyloid; DEG, differentially expressed genes; DISC1, Disrupted‐In‐Schizophrenia 1; FDR, false discovery rate; GO, gene ontology; iPSC, induced pluripotent stem cell; TSA, trichostatin‐A.

    Article Snippet: For experimental treatments, neurons were cultured until in vitro day (DIV) 4, at which point they were treated with various concentrations of TSA (TSA, Sigma–Aldrich, cat. #: T1952) and Aβ oligomers (StressMarq, cat. #: SPR‐488).

    Techniques: Derivative Assay, Gene Expression, Control, Expressing

    Differential gene expression analysis of TSA and amyloid‐beta treatment in neural cells. (A) Volcano plot showing the main effect of Aβ treatment on gene expression (Amyloid‐beta Main Effect). Significantly downregulated genes are shown in blue and upregulated genes in red (adjusted p ‐value < 0.05, |log 2 FC| > 0.58). (B) Volcano plot displaying the main effect of TSA treatment on gene expression (TSA Main Effect). Significantly downregulated genes are shown in blue and upregulated genes in red. (C) Volcano plot illustrating the interaction effect between TSA and Aβ treatments (TSA:Amyloid‐beta Interaction Effect). Significantly downregulated genes are shown in blue and upregulated genes in red. (D) Heatmap displaying expression patterns of top differentially expressed genes across experimental conditions, clustered by effect type. Samples are organized by treatment condition: Control, AB (Aβ), TSA, and TSA+AB (Combined). Left sidebar color bars indicate Condition (Control, Amyloid_beta, TSA, Combined). Right sidebar color bars indicate Direction (Up, Down) and Effect (TSA, Amyloid‐beta, Interaction). Expression values are shown as normalized z ‐scores with yellow indicating high expression and blue indicating low expression. Aβ, β‐amyloid; TSA, trichostatin‐A.

    Journal: Alzheimer's & Dementia

    Article Title: Single‐cell analysis reveals neuroprotective histone deacetylase inhibitor pathways

    doi: 10.1002/alz.71108

    Figure Lengend Snippet: Differential gene expression analysis of TSA and amyloid‐beta treatment in neural cells. (A) Volcano plot showing the main effect of Aβ treatment on gene expression (Amyloid‐beta Main Effect). Significantly downregulated genes are shown in blue and upregulated genes in red (adjusted p ‐value < 0.05, |log 2 FC| > 0.58). (B) Volcano plot displaying the main effect of TSA treatment on gene expression (TSA Main Effect). Significantly downregulated genes are shown in blue and upregulated genes in red. (C) Volcano plot illustrating the interaction effect between TSA and Aβ treatments (TSA:Amyloid‐beta Interaction Effect). Significantly downregulated genes are shown in blue and upregulated genes in red. (D) Heatmap displaying expression patterns of top differentially expressed genes across experimental conditions, clustered by effect type. Samples are organized by treatment condition: Control, AB (Aβ), TSA, and TSA+AB (Combined). Left sidebar color bars indicate Condition (Control, Amyloid_beta, TSA, Combined). Right sidebar color bars indicate Direction (Up, Down) and Effect (TSA, Amyloid‐beta, Interaction). Expression values are shown as normalized z ‐scores with yellow indicating high expression and blue indicating low expression. Aβ, β‐amyloid; TSA, trichostatin‐A.

    Article Snippet: For experimental treatments, neurons were cultured until in vitro day (DIV) 4, at which point they were treated with various concentrations of TSA (TSA, Sigma–Aldrich, cat. #: T1952) and Aβ oligomers (StressMarq, cat. #: SPR‐488).

    Techniques: Gene Expression, Expressing, Control