mouse anti human aβ monoclonal antibody 6e10 Search Results


anti mouse  (Vector Laboratories)
95
Vector Laboratories anti mouse
Anti Mouse, supplied by Vector Laboratories, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mouse anti-aβ  (Agilent technologies)
90
Agilent technologies mouse anti-aβ
Tau immunolabelling of the axonal cytoskeleton demonstrated that axonal morphology was similar between wildtype (A) and Tg2576 (B) cortical neurons over 7–14 DIV. Six daily 1 µM <t>Aβ</t> 1-40 treatments of 7DIV wildtype neurons had no discernible effect upon axonal morphology (C). However, substantial changes in tau-labelling were observed in Aβ 1-40 treated Tg2576 neurons (D); including increased intensity of tau immunostaining after 24 hours, followed by blebbing and axonal fragmentation which worsened after four days of treatment (D). Furthermore, after four consecutive days of 1 µM Aβ 1-40 treatment a number of axonal swellings, with dense accumulations <t>of</t> <t>hyperphosphorylated</t> tau, were observed in Tg2576 neuron cultures (E). scale bars = 30 µm (A–D), 15 µm (E).
Mouse Anti Aβ, supplied by Agilent technologies, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mouse on mouse  (Vector Laboratories)
96
Vector Laboratories mouse on mouse
Tau immunolabelling of the axonal cytoskeleton demonstrated that axonal morphology was similar between wildtype (A) and Tg2576 (B) cortical neurons over 7–14 DIV. Six daily 1 µM <t>Aβ</t> 1-40 treatments of 7DIV wildtype neurons had no discernible effect upon axonal morphology (C). However, substantial changes in tau-labelling were observed in Aβ 1-40 treated Tg2576 neurons (D); including increased intensity of tau immunostaining after 24 hours, followed by blebbing and axonal fragmentation which worsened after four days of treatment (D). Furthermore, after four consecutive days of 1 µM Aβ 1-40 treatment a number of axonal swellings, with dense accumulations <t>of</t> <t>hyperphosphorylated</t> tau, were observed in Tg2576 neuron cultures (E). scale bars = 30 µm (A–D), 15 µm (E).
Mouse On Mouse, supplied by Vector Laboratories, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mouse monoclonal antibody 6e10  (Senetek plc)
90
Senetek plc mouse monoclonal antibody 6e10
Tau immunolabelling of the axonal cytoskeleton demonstrated that axonal morphology was similar between wildtype (A) and Tg2576 (B) cortical neurons over 7–14 DIV. Six daily 1 µM <t>Aβ</t> 1-40 treatments of 7DIV wildtype neurons had no discernible effect upon axonal morphology (C). However, substantial changes in tau-labelling were observed in Aβ 1-40 treated Tg2576 neurons (D); including increased intensity of tau immunostaining after 24 hours, followed by blebbing and axonal fragmentation which worsened after four days of treatment (D). Furthermore, after four consecutive days of 1 µM Aβ 1-40 treatment a number of axonal swellings, with dense accumulations <t>of</t> <t>hyperphosphorylated</t> tau, were observed in Tg2576 neuron cultures (E). scale bars = 30 µm (A–D), 15 µm (E).
Mouse Monoclonal Antibody 6e10, supplied by Senetek plc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anti-app 66-81 antibody (clone 22c11) mouse mab348  (Millipore)
90
Millipore anti-app 66-81 antibody (clone 22c11) mouse mab348
Early and selective degeneration of cholinergic afferent inputs is paralleled by the decline of presynaptic markers and loss in polyubiquitin-conjugates in hippocampi from transgenic Tg2576 AD mice, just mirroring the in vitro “dying-back”-like mechanism(s) of NGF-deprived cholinergic neurons. (A–L) Crude synaptosomal preparations of hippocampi representing mainly the presynaptic compartment were isolated from 1-month-old and 9-months-old Tg2576 AD mice and age-matched littermate Wt ( n = 4–6 pooled mice lysates/experimental group) and analyzed by Western blotting for the expression levels of ubiquitin (A) , synapsin I (C) , synaptophysin and syntaxin I (E) , TrkA, ChAT and M1 as cholinergic markers (G) , vGAT, vGLUT1 and NR1 as non-cholinergic markers (I) , β-amyloid monomer/oligomeric species (anti β-amyloid 1-16 antibody, clone <t>6E10),</t> APP holoprotein (Anti-APP 66-81 antibody, clone 22C11) (K) . Bar graphs (B,D,F,H,J) showed the densitometric quantification of immunoreactivity levels normalized by calculating the ratio of the intensity of the signal for the protein of interest to that of β-actin (L) which was used as loading control for each sample/lane. Values were mean ± SEM of at least of five independent experiments and were expressed with respect to corresponding age-matched wild-type counterpart. Statistically significant differences were calculated by unpaired-two tailed t -Student’s test ( ∗ p < 0.05). Notice that glutamatergic and GABAergic neurotransmission were unaffected in this AD animal model despite the increasing aging of mice and the progressive accumulation of soluble Aβ monomeric/oligomeric species. On the contrary, the selective denervation of more vulnerable cholinergic neuronal afferents was just evident in young 1-month-old Tg2576 AD mice when compared to their age-matched littermate wild-type controls.
Anti App 66 81 Antibody (Clone 22c11) Mouse Mab348, supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mouse anti-aβ antibody  (Millipore)
90
Millipore mouse anti-aβ antibody
Early and selective degeneration of cholinergic afferent inputs is paralleled by the decline of presynaptic markers and loss in polyubiquitin-conjugates in hippocampi from transgenic Tg2576 AD mice, just mirroring the in vitro “dying-back”-like mechanism(s) of NGF-deprived cholinergic neurons. (A–L) Crude synaptosomal preparations of hippocampi representing mainly the presynaptic compartment were isolated from 1-month-old and 9-months-old Tg2576 AD mice and age-matched littermate Wt ( n = 4–6 pooled mice lysates/experimental group) and analyzed by Western blotting for the expression levels of ubiquitin (A) , synapsin I (C) , synaptophysin and syntaxin I (E) , TrkA, ChAT and M1 as cholinergic markers (G) , vGAT, vGLUT1 and NR1 as non-cholinergic markers (I) , β-amyloid monomer/oligomeric species (anti β-amyloid 1-16 antibody, clone <t>6E10),</t> APP holoprotein (Anti-APP 66-81 antibody, clone 22C11) (K) . Bar graphs (B,D,F,H,J) showed the densitometric quantification of immunoreactivity levels normalized by calculating the ratio of the intensity of the signal for the protein of interest to that of β-actin (L) which was used as loading control for each sample/lane. Values were mean ± SEM of at least of five independent experiments and were expressed with respect to corresponding age-matched wild-type counterpart. Statistically significant differences were calculated by unpaired-two tailed t -Student’s test ( ∗ p < 0.05). Notice that glutamatergic and GABAergic neurotransmission were unaffected in this AD animal model despite the increasing aging of mice and the progressive accumulation of soluble Aβ monomeric/oligomeric species. On the contrary, the selective denervation of more vulnerable cholinergic neuronal afferents was just evident in young 1-month-old Tg2576 AD mice when compared to their age-matched littermate wild-type controls.
Mouse Anti Aβ Antibody, supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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elisa mouse monoclonal anti-aβ antibodies 6e10  (Covance)
90
Covance elisa mouse monoclonal anti-aβ antibodies 6e10
Early and selective degeneration of cholinergic afferent inputs is paralleled by the decline of presynaptic markers and loss in polyubiquitin-conjugates in hippocampi from transgenic Tg2576 AD mice, just mirroring the in vitro “dying-back”-like mechanism(s) of NGF-deprived cholinergic neurons. (A–L) Crude synaptosomal preparations of hippocampi representing mainly the presynaptic compartment were isolated from 1-month-old and 9-months-old Tg2576 AD mice and age-matched littermate Wt ( n = 4–6 pooled mice lysates/experimental group) and analyzed by Western blotting for the expression levels of ubiquitin (A) , synapsin I (C) , synaptophysin and syntaxin I (E) , TrkA, ChAT and M1 as cholinergic markers (G) , vGAT, vGLUT1 and NR1 as non-cholinergic markers (I) , β-amyloid monomer/oligomeric species (anti β-amyloid 1-16 antibody, clone <t>6E10),</t> APP holoprotein (Anti-APP 66-81 antibody, clone 22C11) (K) . Bar graphs (B,D,F,H,J) showed the densitometric quantification of immunoreactivity levels normalized by calculating the ratio of the intensity of the signal for the protein of interest to that of β-actin (L) which was used as loading control for each sample/lane. Values were mean ± SEM of at least of five independent experiments and were expressed with respect to corresponding age-matched wild-type counterpart. Statistically significant differences were calculated by unpaired-two tailed t -Student’s test ( ∗ p < 0.05). Notice that glutamatergic and GABAergic neurotransmission were unaffected in this AD animal model despite the increasing aging of mice and the progressive accumulation of soluble Aβ monomeric/oligomeric species. On the contrary, the selective denervation of more vulnerable cholinergic neuronal afferents was just evident in young 1-month-old Tg2576 AD mice when compared to their age-matched littermate wild-type controls.
Elisa Mouse Monoclonal Anti Aβ Antibodies 6e10, supplied by Covance, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mouse anti-aβ protein (6e10) antibody  (Millipore)
90
Millipore mouse anti-aβ protein (6e10) antibody
Early and selective degeneration of cholinergic afferent inputs is paralleled by the decline of presynaptic markers and loss in polyubiquitin-conjugates in hippocampi from transgenic Tg2576 AD mice, just mirroring the in vitro “dying-back”-like mechanism(s) of NGF-deprived cholinergic neurons. (A–L) Crude synaptosomal preparations of hippocampi representing mainly the presynaptic compartment were isolated from 1-month-old and 9-months-old Tg2576 AD mice and age-matched littermate Wt ( n = 4–6 pooled mice lysates/experimental group) and analyzed by Western blotting for the expression levels of ubiquitin (A) , synapsin I (C) , synaptophysin and syntaxin I (E) , TrkA, ChAT and M1 as cholinergic markers (G) , vGAT, vGLUT1 and NR1 as non-cholinergic markers (I) , β-amyloid monomer/oligomeric species (anti β-amyloid 1-16 antibody, clone <t>6E10),</t> APP holoprotein (Anti-APP 66-81 antibody, clone 22C11) (K) . Bar graphs (B,D,F,H,J) showed the densitometric quantification of immunoreactivity levels normalized by calculating the ratio of the intensity of the signal for the protein of interest to that of β-actin (L) which was used as loading control for each sample/lane. Values were mean ± SEM of at least of five independent experiments and were expressed with respect to corresponding age-matched wild-type counterpart. Statistically significant differences were calculated by unpaired-two tailed t -Student’s test ( ∗ p < 0.05). Notice that glutamatergic and GABAergic neurotransmission were unaffected in this AD animal model despite the increasing aging of mice and the progressive accumulation of soluble Aβ monomeric/oligomeric species. On the contrary, the selective denervation of more vulnerable cholinergic neuronal afferents was just evident in young 1-month-old Tg2576 AD mice when compared to their age-matched littermate wild-type controls.
Mouse Anti Aβ Protein (6e10) Antibody, supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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oregon green 488-conjugated anti-mouse igg  (Thermo Fisher)
90
Thermo Fisher oregon green 488-conjugated anti-mouse igg
Early and selective degeneration of cholinergic afferent inputs is paralleled by the decline of presynaptic markers and loss in polyubiquitin-conjugates in hippocampi from transgenic Tg2576 AD mice, just mirroring the in vitro “dying-back”-like mechanism(s) of NGF-deprived cholinergic neurons. (A–L) Crude synaptosomal preparations of hippocampi representing mainly the presynaptic compartment were isolated from 1-month-old and 9-months-old Tg2576 AD mice and age-matched littermate Wt ( n = 4–6 pooled mice lysates/experimental group) and analyzed by Western blotting for the expression levels of ubiquitin (A) , synapsin I (C) , synaptophysin and syntaxin I (E) , TrkA, ChAT and M1 as cholinergic markers (G) , vGAT, vGLUT1 and NR1 as non-cholinergic markers (I) , β-amyloid monomer/oligomeric species (anti β-amyloid 1-16 antibody, clone <t>6E10),</t> APP holoprotein (Anti-APP 66-81 antibody, clone 22C11) (K) . Bar graphs (B,D,F,H,J) showed the densitometric quantification of immunoreactivity levels normalized by calculating the ratio of the intensity of the signal for the protein of interest to that of β-actin (L) which was used as loading control for each sample/lane. Values were mean ± SEM of at least of five independent experiments and were expressed with respect to corresponding age-matched wild-type counterpart. Statistically significant differences were calculated by unpaired-two tailed t -Student’s test ( ∗ p < 0.05). Notice that glutamatergic and GABAergic neurotransmission were unaffected in this AD animal model despite the increasing aging of mice and the progressive accumulation of soluble Aβ monomeric/oligomeric species. On the contrary, the selective denervation of more vulnerable cholinergic neuronal afferents was just evident in young 1-month-old Tg2576 AD mice when compared to their age-matched littermate wild-type controls.
Oregon Green 488 Conjugated Anti Mouse Igg, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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immunohistochemical ihc staining  (Bio-Rad)
93
Bio-Rad immunohistochemical ihc staining
Early and selective degeneration of cholinergic afferent inputs is paralleled by the decline of presynaptic markers and loss in polyubiquitin-conjugates in hippocampi from transgenic Tg2576 AD mice, just mirroring the in vitro “dying-back”-like mechanism(s) of NGF-deprived cholinergic neurons. (A–L) Crude synaptosomal preparations of hippocampi representing mainly the presynaptic compartment were isolated from 1-month-old and 9-months-old Tg2576 AD mice and age-matched littermate Wt ( n = 4–6 pooled mice lysates/experimental group) and analyzed by Western blotting for the expression levels of ubiquitin (A) , synapsin I (C) , synaptophysin and syntaxin I (E) , TrkA, ChAT and M1 as cholinergic markers (G) , vGAT, vGLUT1 and NR1 as non-cholinergic markers (I) , β-amyloid monomer/oligomeric species (anti β-amyloid 1-16 antibody, clone <t>6E10),</t> APP holoprotein (Anti-APP 66-81 antibody, clone 22C11) (K) . Bar graphs (B,D,F,H,J) showed the densitometric quantification of immunoreactivity levels normalized by calculating the ratio of the intensity of the signal for the protein of interest to that of β-actin (L) which was used as loading control for each sample/lane. Values were mean ± SEM of at least of five independent experiments and were expressed with respect to corresponding age-matched wild-type counterpart. Statistically significant differences were calculated by unpaired-two tailed t -Student’s test ( ∗ p < 0.05). Notice that glutamatergic and GABAergic neurotransmission were unaffected in this AD animal model despite the increasing aging of mice and the progressive accumulation of soluble Aβ monomeric/oligomeric species. On the contrary, the selective denervation of more vulnerable cholinergic neuronal afferents was just evident in young 1-month-old Tg2576 AD mice when compared to their age-matched littermate wild-type controls.
Immunohistochemical Ihc Staining, supplied by Bio-Rad, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mouse anti-aβ monoclonal antibody 6e10  (MyBiosource Biotechnology)
90
MyBiosource Biotechnology mouse anti-aβ monoclonal antibody 6e10
Early and selective degeneration of cholinergic afferent inputs is paralleled by the decline of presynaptic markers and loss in polyubiquitin-conjugates in hippocampi from transgenic Tg2576 AD mice, just mirroring the in vitro “dying-back”-like mechanism(s) of NGF-deprived cholinergic neurons. (A–L) Crude synaptosomal preparations of hippocampi representing mainly the presynaptic compartment were isolated from 1-month-old and 9-months-old Tg2576 AD mice and age-matched littermate Wt ( n = 4–6 pooled mice lysates/experimental group) and analyzed by Western blotting for the expression levels of ubiquitin (A) , synapsin I (C) , synaptophysin and syntaxin I (E) , TrkA, ChAT and M1 as cholinergic markers (G) , vGAT, vGLUT1 and NR1 as non-cholinergic markers (I) , β-amyloid monomer/oligomeric species (anti β-amyloid 1-16 antibody, clone <t>6E10),</t> APP holoprotein (Anti-APP 66-81 antibody, clone 22C11) (K) . Bar graphs (B,D,F,H,J) showed the densitometric quantification of immunoreactivity levels normalized by calculating the ratio of the intensity of the signal for the protein of interest to that of β-actin (L) which was used as loading control for each sample/lane. Values were mean ± SEM of at least of five independent experiments and were expressed with respect to corresponding age-matched wild-type counterpart. Statistically significant differences were calculated by unpaired-two tailed t -Student’s test ( ∗ p < 0.05). Notice that glutamatergic and GABAergic neurotransmission were unaffected in this AD animal model despite the increasing aging of mice and the progressive accumulation of soluble Aβ monomeric/oligomeric species. On the contrary, the selective denervation of more vulnerable cholinergic neuronal afferents was just evident in young 1-month-old Tg2576 AD mice when compared to their age-matched littermate wild-type controls.
Mouse Anti Aβ Monoclonal Antibody 6e10, supplied by MyBiosource Biotechnology, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anti-aβ1−17 (6e10 antibody, mouse monoclonal human aβ protein, 1:5000  (Signet Testing)
90
Signet Testing anti-aβ1−17 (6e10 antibody, mouse monoclonal human aβ protein, 1:5000
Early and selective degeneration of cholinergic afferent inputs is paralleled by the decline of presynaptic markers and loss in polyubiquitin-conjugates in hippocampi from transgenic Tg2576 AD mice, just mirroring the in vitro “dying-back”-like mechanism(s) of NGF-deprived cholinergic neurons. (A–L) Crude synaptosomal preparations of hippocampi representing mainly the presynaptic compartment were isolated from 1-month-old and 9-months-old Tg2576 AD mice and age-matched littermate Wt ( n = 4–6 pooled mice lysates/experimental group) and analyzed by Western blotting for the expression levels of ubiquitin (A) , synapsin I (C) , synaptophysin and syntaxin I (E) , TrkA, ChAT and M1 as cholinergic markers (G) , vGAT, vGLUT1 and NR1 as non-cholinergic markers (I) , β-amyloid monomer/oligomeric species (anti β-amyloid 1-16 antibody, clone <t>6E10),</t> APP holoprotein (Anti-APP 66-81 antibody, clone 22C11) (K) . Bar graphs (B,D,F,H,J) showed the densitometric quantification of immunoreactivity levels normalized by calculating the ratio of the intensity of the signal for the protein of interest to that of β-actin (L) which was used as loading control for each sample/lane. Values were mean ± SEM of at least of five independent experiments and were expressed with respect to corresponding age-matched wild-type counterpart. Statistically significant differences were calculated by unpaired-two tailed t -Student’s test ( ∗ p < 0.05). Notice that glutamatergic and GABAergic neurotransmission were unaffected in this AD animal model despite the increasing aging of mice and the progressive accumulation of soluble Aβ monomeric/oligomeric species. On the contrary, the selective denervation of more vulnerable cholinergic neuronal afferents was just evident in young 1-month-old Tg2576 AD mice when compared to their age-matched littermate wild-type controls.
Anti Aβ1−17 (6e10 Antibody, Mouse Monoclonal Human Aβ Protein, 1:5000, supplied by Signet Testing, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Tau immunolabelling of the axonal cytoskeleton demonstrated that axonal morphology was similar between wildtype (A) and Tg2576 (B) cortical neurons over 7–14 DIV. Six daily 1 µM Aβ 1-40 treatments of 7DIV wildtype neurons had no discernible effect upon axonal morphology (C). However, substantial changes in tau-labelling were observed in Aβ 1-40 treated Tg2576 neurons (D); including increased intensity of tau immunostaining after 24 hours, followed by blebbing and axonal fragmentation which worsened after four days of treatment (D). Furthermore, after four consecutive days of 1 µM Aβ 1-40 treatment a number of axonal swellings, with dense accumulations of hyperphosphorylated tau, were observed in Tg2576 neuron cultures (E). scale bars = 30 µm (A–D), 15 µm (E).

Journal: PLoS ONE

Article Title: Tg2576 Cortical Neurons That Express Human Ab Are Susceptible to Extracellular Aβ-Induced, K + Efflux Dependent Neurodegeneration

doi: 10.1371/journal.pone.0019026

Figure Lengend Snippet: Tau immunolabelling of the axonal cytoskeleton demonstrated that axonal morphology was similar between wildtype (A) and Tg2576 (B) cortical neurons over 7–14 DIV. Six daily 1 µM Aβ 1-40 treatments of 7DIV wildtype neurons had no discernible effect upon axonal morphology (C). However, substantial changes in tau-labelling were observed in Aβ 1-40 treated Tg2576 neurons (D); including increased intensity of tau immunostaining after 24 hours, followed by blebbing and axonal fragmentation which worsened after four days of treatment (D). Furthermore, after four consecutive days of 1 µM Aβ 1-40 treatment a number of axonal swellings, with dense accumulations of hyperphosphorylated tau, were observed in Tg2576 neuron cultures (E). scale bars = 30 µm (A–D), 15 µm (E).

Article Snippet: For immunocytochemistry, rabbit anti-tau (1∶5000; DAKO), mouse anti-Aβ (6E10; 1∶1000; DAKO) and mouse anti-hyperphosphorylated tau (AT-8; 1∶1000; Chemicon) antibodies were applied, and detected with appropriate Alexa-Fluor-488 or -594 conjugated secondary antibodies at a 1∶1000 concentration (Molecular Probes).

Techniques: Immunostaining

Early and selective degeneration of cholinergic afferent inputs is paralleled by the decline of presynaptic markers and loss in polyubiquitin-conjugates in hippocampi from transgenic Tg2576 AD mice, just mirroring the in vitro “dying-back”-like mechanism(s) of NGF-deprived cholinergic neurons. (A–L) Crude synaptosomal preparations of hippocampi representing mainly the presynaptic compartment were isolated from 1-month-old and 9-months-old Tg2576 AD mice and age-matched littermate Wt ( n = 4–6 pooled mice lysates/experimental group) and analyzed by Western blotting for the expression levels of ubiquitin (A) , synapsin I (C) , synaptophysin and syntaxin I (E) , TrkA, ChAT and M1 as cholinergic markers (G) , vGAT, vGLUT1 and NR1 as non-cholinergic markers (I) , β-amyloid monomer/oligomeric species (anti β-amyloid 1-16 antibody, clone 6E10), APP holoprotein (Anti-APP 66-81 antibody, clone 22C11) (K) . Bar graphs (B,D,F,H,J) showed the densitometric quantification of immunoreactivity levels normalized by calculating the ratio of the intensity of the signal for the protein of interest to that of β-actin (L) which was used as loading control for each sample/lane. Values were mean ± SEM of at least of five independent experiments and were expressed with respect to corresponding age-matched wild-type counterpart. Statistically significant differences were calculated by unpaired-two tailed t -Student’s test ( ∗ p < 0.05). Notice that glutamatergic and GABAergic neurotransmission were unaffected in this AD animal model despite the increasing aging of mice and the progressive accumulation of soluble Aβ monomeric/oligomeric species. On the contrary, the selective denervation of more vulnerable cholinergic neuronal afferents was just evident in young 1-month-old Tg2576 AD mice when compared to their age-matched littermate wild-type controls.

Journal: Frontiers in Cellular Neuroscience

Article Title: NGF-Dependent Changes in Ubiquitin Homeostasis Trigger Early Cholinergic Degeneration in Cellular and Animal AD-Model

doi: 10.3389/fncel.2018.00487

Figure Lengend Snippet: Early and selective degeneration of cholinergic afferent inputs is paralleled by the decline of presynaptic markers and loss in polyubiquitin-conjugates in hippocampi from transgenic Tg2576 AD mice, just mirroring the in vitro “dying-back”-like mechanism(s) of NGF-deprived cholinergic neurons. (A–L) Crude synaptosomal preparations of hippocampi representing mainly the presynaptic compartment were isolated from 1-month-old and 9-months-old Tg2576 AD mice and age-matched littermate Wt ( n = 4–6 pooled mice lysates/experimental group) and analyzed by Western blotting for the expression levels of ubiquitin (A) , synapsin I (C) , synaptophysin and syntaxin I (E) , TrkA, ChAT and M1 as cholinergic markers (G) , vGAT, vGLUT1 and NR1 as non-cholinergic markers (I) , β-amyloid monomer/oligomeric species (anti β-amyloid 1-16 antibody, clone 6E10), APP holoprotein (Anti-APP 66-81 antibody, clone 22C11) (K) . Bar graphs (B,D,F,H,J) showed the densitometric quantification of immunoreactivity levels normalized by calculating the ratio of the intensity of the signal for the protein of interest to that of β-actin (L) which was used as loading control for each sample/lane. Values were mean ± SEM of at least of five independent experiments and were expressed with respect to corresponding age-matched wild-type counterpart. Statistically significant differences were calculated by unpaired-two tailed t -Student’s test ( ∗ p < 0.05). Notice that glutamatergic and GABAergic neurotransmission were unaffected in this AD animal model despite the increasing aging of mice and the progressive accumulation of soluble Aβ monomeric/oligomeric species. On the contrary, the selective denervation of more vulnerable cholinergic neuronal afferents was just evident in young 1-month-old Tg2576 AD mice when compared to their age-matched littermate wild-type controls.

Article Snippet: The following antibodies were used: anti-ubiquitin antibody rabbit Z0458 Dako-Cytomation; anti-synapsin I antibody rabbit AB1543P Millipore; anti-SNAP25 antibody (clone SMI 81) mouse 836301 BioLegend; anti-α-synuclein antibody (clone 42) mouse 610786 BD Transduction Laboratories; anti-synaptophysin antibody (D-4) mouse sc-17750 Santa Cruz; anti-syntaxin 1 mouse S1172 Sigma-Aldrich; anti-TrkA antibody (763) rabbit sc-118 Santa Cruz; anti-choactase antibody (H-95) rabbit sc-20672 Santa Cruz; anti-mAChR M1 antibody (H120) rabbit sc-9106 Santa Cruz; anti-vGLUT1 antibody rabbit 135 302 Synaptic System; anti-vGAT antibody rabbit 131 003 Synaptic System; NMDAζ1 antibody (C-20) goat sc-1467 Santa Cruz; anti-β-Amyloid 1-16 antibody (clone 6E10) mouse Signet 932002; anti-APP 66-81 antibody (clone 22C11) mouse MAB348 Millipore; anti-LC-3 pAb antibody rabbit PD014 MBL; anti-β-actin antibody mouse S3062 Sigma-Aldrich; anti-UCHL-1 (C-4) antibody mouse sc-271639 Santa Cruz; anti-mouse IgG (whole molecule)-Peroxidase antibody A4416 Sigma-Aldrich; anti-rabbit IgG (whole molecule)-Peroxidase antibody A9169 Sigma-Aldrich; donkey anti-goat IgG-HRP antibody sc2056 Santa Cruz.

Techniques: Transgenic Assay, In Vitro, Isolation, Western Blot, Expressing, Ubiquitin Proteomics, Control, Two Tailed Test, Animal Model