mouse monoclonal antibody at180  (Thermo Fisher)

Journal: Scientific Reports

Article Title: A novel pThr217 tau monoclonal antibody reveals neuropathological heterogeneity in tauopathies

doi: 10.1038/s41598-025-04291-y

Figure Lengend Snippet: Immunohistochemical labelling of Alzheimer’s disease neuropathology. Immunohistochemical staining was performed as described in the “Materials and methods”. (a) Staining of AD and control frontal cortex tissue using monoclonal antibodies 7F2, AT180, 1F10, and AT100 is shown. Thin arrows indicate NFTs, arrow heads demonstrate neuritic plaques, thick arrows highlight neuropil threads. Scale bar of low magnification images is 100 μm, inset is 15 μm. (b) Semi-quantitative analysis of AD tau pathology in the frontal cortex is described in the “Materials and methods”. Data is presented as mean +/- SEM.

Article Snippet: AT180 is a mouse monoclonal antibody specific for tau phosphorylated at Thr231 , was purchased from Thermo Fisher Scientific (Waltham, MA, USA).

Techniques: Immunohistochemical staining, Staining, Control, Bioprocessing

Journal: Scientific Reports

Article Title: A novel pThr217 tau monoclonal antibody reveals neuropathological heterogeneity in tauopathies

doi: 10.1038/s41598-025-04291-y

Figure Lengend Snippet: Immunohistochemical labelling of PSP and CBD neuropathology. Immunohistochemical staining was performed as described in the “Materials and methods”. (a) Staining of PSP and CBD striatal tissue using monoclonal antibodies 7F2, AT180, and 1F10 is shown. Scale bar is 80 μm. (b) Semi-quantitative analysis of PSP and CBD tau pathology in the caudate and putamen is described in the “Materials and methods”. Data is presented as mean +/- SEM.

Article Snippet: AT180 is a mouse monoclonal antibody specific for tau phosphorylated at Thr231 , was purchased from Thermo Fisher Scientific (Waltham, MA, USA).

Techniques: Immunohistochemical staining, Staining, Bioprocessing

Journal: Scientific Reports

Article Title: A novel pThr217 tau monoclonal antibody reveals neuropathological heterogeneity in tauopathies

doi: 10.1038/s41598-025-04291-y

Figure Lengend Snippet: Immunohistochemical labelling of PiD neuropathology. Immunohistochemical staining was performed as described in the “Materials and methods”. Staining of PiD hippocampal tissue using antibodies 7F2, AT180, and 1F10 is shown. Scale bar of low magnification images is 100 μm, inset is 15 μm.

Article Snippet: AT180 is a mouse monoclonal antibody specific for tau phosphorylated at Thr231 , was purchased from Thermo Fisher Scientific (Waltham, MA, USA).

Techniques: Immunohistochemical staining, Staining

Journal: Frontiers in Cellular Neuroscience

Article Title: APPsα rescues CDK5 and GSK3β dysregulation and restores normal spine density in Tau transgenic mice

doi: 10.3389/fncel.2023.1106176

Figure Lengend Snippet: Progressive Tau pathology in the hippocampus of THY-Tau22 mice. (A–D) Distinct antibodies were used to detect total human Tau (HT7), misfolded Tau (MC1), PHFs and phospho-Tau (AT8 and AT180) at 3, 6, 9, and 12 months of age in hippocampi of THY-Tau22 mice. Exemplary images are shown for 3 (left) and 9 months (middle). Quantification of immunoreactivity over time (right): immunoreactivity for each antibody was measured in three layers of the CA1 region (stratum oriens = O; stratum pyramidale = P; and stratum radiatum = R), by placing rectangles into each area and measuring mean fluorescence intensities (MFI), as shown for HT7 staining at 3 months [ (A) , left]. Staining intensity in the CA1 layers was quantified relative to staining intensity of wild type controls (set as 100%). For the first time point (3 months of age), significant differences are indicated relative to wild type controls. For subsequent time points (6, 9, and 12 months of age) differences in immunoreactivity in THY-Tau22 sections were calculated relative to the proceeding time point to asses age-dependent differences in each of the layers analyzed. (A) At 3 months HT7 + immunoreactivity was present in all subfields (CA1, CA3, and DG) of the hippocampus (left). At 9 months signal intensity increased in all subfields (middle), leading to a significant increase in the mean pixel intensities for all subfields over time (right). (B) At 3 months misfolded Tau species (MC1 + ) were mainly detected in the polymorph layer (po) of the DG, the stratum lucidum (sl) and the distal stratum pyramidale (P) of CA1 (left). At 9 months the number of MC1 + cells located in CA1 region was increased (middle), resulting in increased MFIs in O and P (right). (C) At 3 months only weak AT8 + immunoreactivity was detectable, with few scattered positive cells in the CA1 region (left). At 9 months AT8 + immunoreactivity was detectable in dentate granule cells and was dramatically increased in CA1 pyramidal cells (middle), resulting in increased MFIs in O and P (right). (D) At 3 months of age, AT180 + immunoreactivity was prominent in all hippocampal subfields (left) and was even more enhanced at later time-points (9 months, middle). Quantification indicated a progressive increase from 3 to 12 months of age in all layers (right). (E) Microglia (IBA1) were present in a regularly distributed pattern all over the hippocampus with no obvious changes in morphology or distribution over time (left and middle), despite a slight increase in MFI at 12 months compared to 6 months of age (right). Note that no analysis was performed for IBA and GFAP at 9 months of age. (F) With exception for the stratum pyramidale and stratum granulosum (sg), also astroglia (GFAP) were regularly distributed over the whole hippocampus. From 3 to 6 months of age there was a significant increase in GFAP immunoreactivity. Data are depicted as mean ± SEM. MFIs in sublayers were analyzed using one-way ANOVA with Bonferroni’s post hoc test: * p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001, **** p ≤ 0.0001. All images were captured with the same laser intensity, avoiding overexposure. N = 3–5 animals per genotype and age, n = 6–15 analyzed areas; images depict maximum intensity projections taken from 40 μm coronal sections, scale bars: 500 μm.

Article Snippet: Sections were incubated in 50 mM NH 4 CL for 15 min, neutralizing remaining PFA, before they were washed in PBS and permeabilized (2% Triton X-100 in PBS) overnight, followed by a blocking step [M.O.M. (Mouse on Mouse) Blocking Reagent, 1:100, #MKB-2213, Vector Laboratories] for 6 h. After washing, sections were incubated with the following primary antibodies in PBS with 5% NGS: HT7 (mouse monoclonal, 1:200, #MN1000, Thermo Fisher Scientific), AT8 (mouse monoclonal, 1:200, #MN1020, Thermo Fisher Scientific), AT180 (mouse monoclonal, 1:200, #MN1040, Thermo Fisher Scientific), MC1 (mouse monoclonal, 1:50, kindly provided by Peter Davies).

Techniques: Fluorescence, Staining

Journal: The European Journal of Neuroscience

Article Title: Alzheimer's disease‐like neuropathology in three species of oceanic dolphin

doi: 10.1111/ejn.15900

Figure Lengend Snippet: Abundance and distribution of phosphorylated tau protein (pTau), detected by antibody AT180, in all available sections of the brains of three odontocetes (Gm1, La5 and Tt1) with amyloid plaques present and one (Gm5) with no amyloid plaques present, and the two selected sections of cerebral cortex from the four younger, control, odontocetes (Gm6, Gm7, La6 and Tt2)

Article Snippet: To localize pTau, mouse monoclonal antibodies raised against Phospho‐Tau (Thr231) [AT180] (MN1040, ThermoFisher, Renfrew, UK), which labels pre‐NFTs and so would be expected to detect early‐stage AD‐like pathology, and antibodies raised against Phospho‐Tau (Ser202, Thr205) [AT8] (MN1020, ThermoFisher), which detects well‐developed NFTs present in later‐stage AD‐like pathology, were used, both diluted 1:1000 in 5% NGS/PBST and applied to separate semi‐serial sections.

Techniques: Control

Journal: The European Journal of Neuroscience

Article Title: Alzheimer's disease‐like neuropathology in three species of oceanic dolphin

doi: 10.1111/ejn.15900

Figure Lengend Snippet: Immunolabelling (brown pigment) of phosphorylated tau protein (pTau) using antibody AT180 in the cerebral cortices of odontocetes. When at lower intensities, immunolabelling of pTau was present as cytoplasmic granules within the cell bodies of neurons (a), and with increased intensity of labelling, pTau frequently extended into the axons and dendrites (b,c). Irrespective of the intensity of cytoplasmic labelling, nuclei were consistently devoid of any labelling (c) although neurons that labelled intensely for pTau frequently contained pyknotic nuclei (d, arrowhead). Intensely phospho‐tau‐stained cells were found in animal (Gm5) and present in all sections of cerebral cortex available for examination (e,f). Neuritic plaques were present in both the white and grey matter in all four aged animals examined (Gm1, Gm5, La5 and Tt1) and within the grey matter often colocalized with neuropil threads (g, arrowhead). Similarly, neuritic plaques colocalized with phospho‐tau‐positive cell bodies (h,i, arrowheads). pTau labelling was present predominantly in cerebrocortical layers II and V (j). Positive control sections were composed of human brain tissue from a case of definitely diagnosed Alzheimer's disease (k). Semi‐serial sections were used for the controls (k, positive; l, negative control)

Article Snippet: To localize pTau, mouse monoclonal antibodies raised against Phospho‐Tau (Thr231) [AT180] (MN1040, ThermoFisher, Renfrew, UK), which labels pre‐NFTs and so would be expected to detect early‐stage AD‐like pathology, and antibodies raised against Phospho‐Tau (Ser202, Thr205) [AT8] (MN1020, ThermoFisher), which detects well‐developed NFTs present in later‐stage AD‐like pathology, were used, both diluted 1:1000 in 5% NGS/PBST and applied to separate semi‐serial sections.

Techniques: Staining, Positive Control, Negative Control

Journal: The European Journal of Neuroscience

Article Title: Alzheimer's disease‐like neuropathology in three species of oceanic dolphin

doi: 10.1111/ejn.15900

Figure Lengend Snippet: Phosphorylated tau (pTau) localized using antibody AT180 (brown pigment), in a young bottlenose dolphin (Tt2). pTau was present within neuropil of the white matter but not the grey matter (a). It was also present in the cytoplasm of nearly all neurons in the cerebrocortical grey matter but absent from the nuclei and surrounding neuropil (b). Furthermore, it was present within the neuropil of the white matter of the supralimbic/paralimbic/limbic lobes of the cortex and the cytoplasm of neurons contained within it (c). Greater magnification of cerebrocortical white matter highlighted the intense cytoplasmic labelling of neurons for pTau while sparing their nuclei (d)

Article Snippet: To localize pTau, mouse monoclonal antibodies raised against Phospho‐Tau (Thr231) [AT180] (MN1040, ThermoFisher, Renfrew, UK), which labels pre‐NFTs and so would be expected to detect early‐stage AD‐like pathology, and antibodies raised against Phospho‐Tau (Ser202, Thr205) [AT8] (MN1020, ThermoFisher), which detects well‐developed NFTs present in later‐stage AD‐like pathology, were used, both diluted 1:1000 in 5% NGS/PBST and applied to separate semi‐serial sections.

Techniques: