Amyloid Plaque

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Reinhard Schliebs - One of the best experts on this subject based on the ideXlab platform.

  • Developmental and Amyloid Plaque-related changes in cerebral cortical capillaries in transgenic Tg2576 Alzheimer mice.
    International Journal of Developmental Neuroscience, 2006
    Co-Authors: Elena Kouznetsova, Margrit Klingner, Dietlind Sorger, Osama Sabri, Udo Grossmann, Jörg Steinbach, Matthias Scheunemann, Reinhard Schliebs
    Abstract:

    Abstract There is experimental evidence that cerebral perfusion is decreased during aging and in Alzheimer's disease. To characterize the temporal relationship between Amyloid deposition, Plaque size and cerebrovascular abnormalities, a semiquantitative immunohistochemical study was performed in transgenic Tg2576 mice that express the Swedish double mutation of human Amyloid precursor protein (APP) and progressively develop Alzheimer-like β-Amyloid deposits. Cortical cryocut sections, obtained from mice at ages ranging between 4 and 18 months, were immunostained to label glucose transporter type 1 (GLUT1), a marker of vascular endothelial cells, and thioflavine-S to visualize Plaques. Regardless of age and transgene, a laminar distribution of capillaries was observed being highest in cortical layers IV and V. The density of microvessels estimated in cortical regions with high Plaque load was found to be significantly lower as compared to areas with low Plaque load. Around large thioflavine-S-positive senile Plaques the capillary density was low, while diffuse Plaques demonstrated a close association of capillaries with no signs of any damage. The data suggest that Amyloid Plaque deposition differentially affects the cerebrovascular system in an age- and Plaque type-related manner, and provide further evidence that β-Amyloid, in addition to its well-described neurotoxic effects, may also contribute to neuronal dysfunction through its actions on the cerebrovasculature.

  • Developmental and Amyloid Plaque-related changes in cerebral cortical capillaries in transgenic Tg2576 Alzheimer mice.
    International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience, 2006
    Co-Authors: Elena Kouznetsova, Margrit Klingner, Dietlind Sorger, Osama Sabri, Udo Grossmann, Jörg Steinbach, Matthias Scheunemann, Reinhard Schliebs
    Abstract:

    There is experimental evidence that cerebral perfusion is decreased during aging and in Alzheimer's disease. To characterize the temporal relationship between Amyloid deposition, Plaque size and cerebrovascular abnormalities, a semiquantitative immunohistochemical study was performed in transgenic Tg2576 mice that express the Swedish double mutation of human Amyloid precursor protein (APP) and progressively develop Alzheimer-like beta-Amyloid deposits. Cortical cryocut sections, obtained from mice at ages ranging between 4 and 18 months, were immunostained to label glucose transporter type 1 (GLUT1), a marker of vascular endothelial cells, and thioflavine-S to visualize Plaques. Regardless of age and transgene, a laminar distribution of capillaries was observed being highest in cortical layers IV and V. The density of microvessels estimated in cortical regions with high Plaque load was found to be significantly lower as compared to areas with low Plaque load. Around large thioflavine-S-positive senile Plaques the capillary density was low, while diffuse Plaques demonstrated a close association of capillaries with no signs of any damage. The data suggest that Amyloid Plaque deposition differentially affects the cerebrovascular system in an age- and Plaque type-related manner, and provide further evidence that beta-Amyloid, in addition to its well-described neurotoxic effects, may also contribute to neuronal dysfunction through its actions on the cerebrovasculature.

  • aging related increase in oxidative stress correlates with developmental pattern of beta secretase activity and beta Amyloid Plaque formation in transgenic tg2576 mice with alzheimer like pathology
    International Journal of Developmental Neuroscience, 2004
    Co-Authors: Jenny Apelt, Marina Bigl, Patrick Wunderlich, Reinhard Schliebs
    Abstract:

    Abstract The molecular mechanisms of β-Amyloidogenesis in sporadic Alzheimer’s disease are still poorly understood. To reveal whether aging-associated increases in brain oxidative stress and inflammation may trigger onset or progression of β-Amyloid deposition, a transgenic mouse (Tg2576) that express the Swedish double mutation of human Amyloid precursor protein (APP) was used as animal model to study the developmental pattern of markers of oxidative stress and APP processing. In Tg2576 mouse brain, cortical levels of soluble β-Amyloid (1–40) and (1–42) steadily increased with age, but significant deposition of fibrillary β-Amyloid in cortical areas did not occur before postnatal age of 10 months. The slope of increase in cerebral cortical β-secretase (BACE1) activities in Tg2576 mice between ages of 9 and 13 months was significantly higher as compared to that of the α-secretase, while the expression level of BACE1 protein and mRNA did not change with age. The activities of superoxide dismutase and glutathione peroxidase in cortical tissue from Tg2576 mice steadily increased from postnatal age 9–12 months. The levels of cortical nitric oxide, and reactive nitrogen species demonstrated peak values around 9 months of age, while the level of interleukin-1β steadily increased from postnatal month 13 onwards. The developmental temporal coincidence of increased levels of reactive nitrogen species and antioxidative enzymes with the onset of β-Amyloid Plaque deposition provides further evidence that developmentally and aging-induced alterations in brain oxidative status exhibit a major factor in triggering enhanced production and deposition of β-Amyloid, and potentially predispose to Alzheimer’s disease.

  • Aging-related increase in oxidative stress correlates with developmental pattern of beta-secretase activity and beta-Amyloid Plaque formation in transgenic Tg2576 mice with Alzheimer-like pathology.
    International Journal of Developmental Neuroscience, 2004
    Co-Authors: Jenny Apelt, Marina Bigl, Patrick Wunderlich, Reinhard Schliebs
    Abstract:

    The molecular mechanisms of beta-Amyloidogenesis in sporadic Alzheimer's disease are still poorly understood. To reveal whether aging-associated increases in brain oxidative stress and inflammation may trigger onset or progression of beta-Amyloid deposition, a transgenic mouse (Tg2576) that express the Swedish double mutation of human Amyloid precursor protein (APP) was used as animal model to study the developmental pattern of markers of oxidative stress and APP processing. In Tg2576 mouse brain, cortical levels of soluble beta-Amyloid (1-40) and (1-42) steadily increased with age, but significant deposition of fibrillary beta-Amyloid in cortical areas did not occur before postnatal age of 10 months. The slope of increase in cerebral cortical beta-secretase (BACE1) activities in Tg2576 mice between ages of 9 and 13 months was significantly higher as compared to that of the alpha-secretase, while the expression level of BACE1 protein and mRNA did not change with age. The activities of superoxide dismutase and glutathione peroxidase in cortical tissue from Tg2576 mice steadily increased from postnatal age 9-12 months. The levels of cortical nitric oxide, and reactive nitrogen species demonstrated peak values around 9 months of age, while the level of interleukin-1beta steadily increased from postnatal month 13 onwards. The developmental temporal coincidence of increased levels of reactive nitrogen species and antioxidative enzymes with the onset of beta-Amyloid Plaque deposition provides further evidence that developmentally and aging-induced alterations in brain oxidative status exhibit a major factor in triggering enhanced production and deposition of beta-Amyloid, and potentially predispose to Alzheimer's disease.

  • alterations in cholinergic and non cholinergic neurotransmitter receptor densities in transgenic tg2576 mouse brain with β Amyloid Plaque pathology
    International Journal of Developmental Neuroscience, 2003
    Co-Authors: Margrit Klingner, Jenny Apelt, Dietlind Sorger, Osama Sabri, Jörg Steinbach, Matthias Scheunemann, Ashok Kumar, Reinhard Schliebs
    Abstract:

    Abstract Cholinergic deficits in Alzheimer’s disease are accompanied by a number of alterations in other transmitter systems including glutamate, noradrenaline and serotonin, suggesting the involvement also of other neurotransmitter systems in the pathogenesis of the disease. To address the question whether β-Amyloid may contribute to these deficits, brain tissue from transgenic Tg2576 mice with Alzheimer Plaque pathology at ages of 5 (still no significant Plaque load) and 17 months (moderate to high cortical β-Amyloid Plaque load) were examined for a number of cholinergic and non-cholinergic markers. Transgenic mice with no significant Plaque load demonstrated reduced hemicholinium-3 (HCh-3) binding to choline uptake sites in anterior brain regions as compared to non-transgenic littermates, while in aged transgenic mice with high number of Plaque deposits decreased HCh-3 binding levels were accompanied by increased vesicular acetylcholine transporter binding in selected cortical brain regions. In aged transgenic mice GABA A , NMDA, AMPA, kainate, and β-adrenergic as well 5-HT 1A - and 5-HT 2A -receptor binding levels were hardly affected, whereas α 1 - and α 2 -adrenoceptor binding was increased in selected cerebral cortical regions as compared to non-transgenic littermates. The development of changes in both cholinergic and non-cholinergic markers in transgenic Tg2576 mouse brain already before the onset of progressive Plaque deposition provides in vivo evidence of a modulatory role of soluble β-Amyloid on cortical neurotransmission and may be referred to the deficits in learning and memory observed in these mice also before significant Plaque load.

Jenny Apelt - One of the best experts on this subject based on the ideXlab platform.

  • aging related increase in oxidative stress correlates with developmental pattern of beta secretase activity and beta Amyloid Plaque formation in transgenic tg2576 mice with alzheimer like pathology
    International Journal of Developmental Neuroscience, 2004
    Co-Authors: Jenny Apelt, Marina Bigl, Patrick Wunderlich, Reinhard Schliebs
    Abstract:

    Abstract The molecular mechanisms of β-Amyloidogenesis in sporadic Alzheimer’s disease are still poorly understood. To reveal whether aging-associated increases in brain oxidative stress and inflammation may trigger onset or progression of β-Amyloid deposition, a transgenic mouse (Tg2576) that express the Swedish double mutation of human Amyloid precursor protein (APP) was used as animal model to study the developmental pattern of markers of oxidative stress and APP processing. In Tg2576 mouse brain, cortical levels of soluble β-Amyloid (1–40) and (1–42) steadily increased with age, but significant deposition of fibrillary β-Amyloid in cortical areas did not occur before postnatal age of 10 months. The slope of increase in cerebral cortical β-secretase (BACE1) activities in Tg2576 mice between ages of 9 and 13 months was significantly higher as compared to that of the α-secretase, while the expression level of BACE1 protein and mRNA did not change with age. The activities of superoxide dismutase and glutathione peroxidase in cortical tissue from Tg2576 mice steadily increased from postnatal age 9–12 months. The levels of cortical nitric oxide, and reactive nitrogen species demonstrated peak values around 9 months of age, while the level of interleukin-1β steadily increased from postnatal month 13 onwards. The developmental temporal coincidence of increased levels of reactive nitrogen species and antioxidative enzymes with the onset of β-Amyloid Plaque deposition provides further evidence that developmentally and aging-induced alterations in brain oxidative status exhibit a major factor in triggering enhanced production and deposition of β-Amyloid, and potentially predispose to Alzheimer’s disease.

  • Aging-related increase in oxidative stress correlates with developmental pattern of beta-secretase activity and beta-Amyloid Plaque formation in transgenic Tg2576 mice with Alzheimer-like pathology.
    International Journal of Developmental Neuroscience, 2004
    Co-Authors: Jenny Apelt, Marina Bigl, Patrick Wunderlich, Reinhard Schliebs
    Abstract:

    The molecular mechanisms of beta-Amyloidogenesis in sporadic Alzheimer's disease are still poorly understood. To reveal whether aging-associated increases in brain oxidative stress and inflammation may trigger onset or progression of beta-Amyloid deposition, a transgenic mouse (Tg2576) that express the Swedish double mutation of human Amyloid precursor protein (APP) was used as animal model to study the developmental pattern of markers of oxidative stress and APP processing. In Tg2576 mouse brain, cortical levels of soluble beta-Amyloid (1-40) and (1-42) steadily increased with age, but significant deposition of fibrillary beta-Amyloid in cortical areas did not occur before postnatal age of 10 months. The slope of increase in cerebral cortical beta-secretase (BACE1) activities in Tg2576 mice between ages of 9 and 13 months was significantly higher as compared to that of the alpha-secretase, while the expression level of BACE1 protein and mRNA did not change with age. The activities of superoxide dismutase and glutathione peroxidase in cortical tissue from Tg2576 mice steadily increased from postnatal age 9-12 months. The levels of cortical nitric oxide, and reactive nitrogen species demonstrated peak values around 9 months of age, while the level of interleukin-1beta steadily increased from postnatal month 13 onwards. The developmental temporal coincidence of increased levels of reactive nitrogen species and antioxidative enzymes with the onset of beta-Amyloid Plaque deposition provides further evidence that developmentally and aging-induced alterations in brain oxidative status exhibit a major factor in triggering enhanced production and deposition of beta-Amyloid, and potentially predispose to Alzheimer's disease.

  • alterations in cholinergic and non cholinergic neurotransmitter receptor densities in transgenic tg2576 mouse brain with β Amyloid Plaque pathology
    International Journal of Developmental Neuroscience, 2003
    Co-Authors: Margrit Klingner, Jenny Apelt, Dietlind Sorger, Osama Sabri, Jörg Steinbach, Matthias Scheunemann, Ashok Kumar, Reinhard Schliebs
    Abstract:

    Abstract Cholinergic deficits in Alzheimer’s disease are accompanied by a number of alterations in other transmitter systems including glutamate, noradrenaline and serotonin, suggesting the involvement also of other neurotransmitter systems in the pathogenesis of the disease. To address the question whether β-Amyloid may contribute to these deficits, brain tissue from transgenic Tg2576 mice with Alzheimer Plaque pathology at ages of 5 (still no significant Plaque load) and 17 months (moderate to high cortical β-Amyloid Plaque load) were examined for a number of cholinergic and non-cholinergic markers. Transgenic mice with no significant Plaque load demonstrated reduced hemicholinium-3 (HCh-3) binding to choline uptake sites in anterior brain regions as compared to non-transgenic littermates, while in aged transgenic mice with high number of Plaque deposits decreased HCh-3 binding levels were accompanied by increased vesicular acetylcholine transporter binding in selected cortical brain regions. In aged transgenic mice GABA A , NMDA, AMPA, kainate, and β-adrenergic as well 5-HT 1A - and 5-HT 2A -receptor binding levels were hardly affected, whereas α 1 - and α 2 -adrenoceptor binding was increased in selected cerebral cortical regions as compared to non-transgenic littermates. The development of changes in both cholinergic and non-cholinergic markers in transgenic Tg2576 mouse brain already before the onset of progressive Plaque deposition provides in vivo evidence of a modulatory role of soluble β-Amyloid on cortical neurotransmission and may be referred to the deficits in learning and memory observed in these mice also before significant Plaque load.

Margrit Klingner - One of the best experts on this subject based on the ideXlab platform.

  • Developmental and Amyloid Plaque-related changes in cerebral cortical capillaries in transgenic Tg2576 Alzheimer mice.
    International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience, 2006
    Co-Authors: Elena Kouznetsova, Margrit Klingner, Dietlind Sorger, Osama Sabri, Udo Grossmann, Jörg Steinbach, Matthias Scheunemann, Reinhard Schliebs
    Abstract:

    There is experimental evidence that cerebral perfusion is decreased during aging and in Alzheimer's disease. To characterize the temporal relationship between Amyloid deposition, Plaque size and cerebrovascular abnormalities, a semiquantitative immunohistochemical study was performed in transgenic Tg2576 mice that express the Swedish double mutation of human Amyloid precursor protein (APP) and progressively develop Alzheimer-like beta-Amyloid deposits. Cortical cryocut sections, obtained from mice at ages ranging between 4 and 18 months, were immunostained to label glucose transporter type 1 (GLUT1), a marker of vascular endothelial cells, and thioflavine-S to visualize Plaques. Regardless of age and transgene, a laminar distribution of capillaries was observed being highest in cortical layers IV and V. The density of microvessels estimated in cortical regions with high Plaque load was found to be significantly lower as compared to areas with low Plaque load. Around large thioflavine-S-positive senile Plaques the capillary density was low, while diffuse Plaques demonstrated a close association of capillaries with no signs of any damage. The data suggest that Amyloid Plaque deposition differentially affects the cerebrovascular system in an age- and Plaque type-related manner, and provide further evidence that beta-Amyloid, in addition to its well-described neurotoxic effects, may also contribute to neuronal dysfunction through its actions on the cerebrovasculature.

  • Developmental and Amyloid Plaque-related changes in cerebral cortical capillaries in transgenic Tg2576 Alzheimer mice.
    International Journal of Developmental Neuroscience, 2006
    Co-Authors: Elena Kouznetsova, Margrit Klingner, Dietlind Sorger, Osama Sabri, Udo Grossmann, Jörg Steinbach, Matthias Scheunemann, Reinhard Schliebs
    Abstract:

    Abstract There is experimental evidence that cerebral perfusion is decreased during aging and in Alzheimer's disease. To characterize the temporal relationship between Amyloid deposition, Plaque size and cerebrovascular abnormalities, a semiquantitative immunohistochemical study was performed in transgenic Tg2576 mice that express the Swedish double mutation of human Amyloid precursor protein (APP) and progressively develop Alzheimer-like β-Amyloid deposits. Cortical cryocut sections, obtained from mice at ages ranging between 4 and 18 months, were immunostained to label glucose transporter type 1 (GLUT1), a marker of vascular endothelial cells, and thioflavine-S to visualize Plaques. Regardless of age and transgene, a laminar distribution of capillaries was observed being highest in cortical layers IV and V. The density of microvessels estimated in cortical regions with high Plaque load was found to be significantly lower as compared to areas with low Plaque load. Around large thioflavine-S-positive senile Plaques the capillary density was low, while diffuse Plaques demonstrated a close association of capillaries with no signs of any damage. The data suggest that Amyloid Plaque deposition differentially affects the cerebrovascular system in an age- and Plaque type-related manner, and provide further evidence that β-Amyloid, in addition to its well-described neurotoxic effects, may also contribute to neuronal dysfunction through its actions on the cerebrovasculature.

  • alterations in cholinergic and non cholinergic neurotransmitter receptor densities in transgenic tg2576 mouse brain with β Amyloid Plaque pathology
    International Journal of Developmental Neuroscience, 2003
    Co-Authors: Margrit Klingner, Jenny Apelt, Dietlind Sorger, Osama Sabri, Jörg Steinbach, Matthias Scheunemann, Ashok Kumar, Reinhard Schliebs
    Abstract:

    Abstract Cholinergic deficits in Alzheimer’s disease are accompanied by a number of alterations in other transmitter systems including glutamate, noradrenaline and serotonin, suggesting the involvement also of other neurotransmitter systems in the pathogenesis of the disease. To address the question whether β-Amyloid may contribute to these deficits, brain tissue from transgenic Tg2576 mice with Alzheimer Plaque pathology at ages of 5 (still no significant Plaque load) and 17 months (moderate to high cortical β-Amyloid Plaque load) were examined for a number of cholinergic and non-cholinergic markers. Transgenic mice with no significant Plaque load demonstrated reduced hemicholinium-3 (HCh-3) binding to choline uptake sites in anterior brain regions as compared to non-transgenic littermates, while in aged transgenic mice with high number of Plaque deposits decreased HCh-3 binding levels were accompanied by increased vesicular acetylcholine transporter binding in selected cortical brain regions. In aged transgenic mice GABA A , NMDA, AMPA, kainate, and β-adrenergic as well 5-HT 1A - and 5-HT 2A -receptor binding levels were hardly affected, whereas α 1 - and α 2 -adrenoceptor binding was increased in selected cerebral cortical regions as compared to non-transgenic littermates. The development of changes in both cholinergic and non-cholinergic markers in transgenic Tg2576 mouse brain already before the onset of progressive Plaque deposition provides in vivo evidence of a modulatory role of soluble β-Amyloid on cortical neurotransmission and may be referred to the deficits in learning and memory observed in these mice also before significant Plaque load.

Wojciech Michno - One of the best experts on this subject based on the ideXlab platform.

  • computational analysis of alzheimer Amyloid Plaque composition in 2d and elastically reconstructed 3d maldi ms images
    Analytical Chemistry, 2020
    Co-Authors: Wojciech Michno, Thomas Enzlein, Jonas Cordes, Bogdan Munteanu, Lutgarde Serneels, Bart De Strooper, Jorg Hanrieder
    Abstract:

    MALDI mass spectrometry imaging (MSI) enables label-free, spatially resolved analysis of a wide range of analytes in tissue sections. Quantitative analysis of MSI datasets is typically performed on single pixels or manually assigned regions of interest (ROIs). However, many sparse, small objects such as Alzheimer's disease (AD) brain deposits of Amyloid peptides called Plaques are neither single pixels nor ROIs. Here, we propose a new approach to facilitate the comparative computational evaluation of Amyloid Plaque-like objects by MSI: a fast Plaque PICKER tool that enables a statistical evaluation of heterogeneous Amyloid peptide composition. Comparing two AD mouse models, APP NL-G-F and APP PS1, we identified distinct heterogeneous Plaque populations in the NL-G-F model but only one class of Plaques in the PS1 model. We propose quantitative metrics for the comparison of technical and biological MSI replicates. Furthermore, we reconstructed a high-accuracy 3D-model of Amyloid Plaques in a fully automated fashion, employing rigid and elastic MSI image registration using structured and Plaque-unrelated reference ion images. Statistical single-Plaque analysis in reconstructed 3D-MSI objects revealed the Aβ1-42Arc peptide to be located either in the core of larger Plaques or in small Plaques without colocalization of other Aβ isoforms. In 3D, a substantially larger number of small Plaques were observed than that indicated by the 2D-MSI data, suggesting that quantitative analysis of molecularly diverse sparsely-distributed features may benefit from 3D-reconstruction. Data are available via ProteomeXchange with identifier PXD020824.

  • multimodal chemical imaging of Amyloid Plaque polymorphism reveals aβ aggregation dependent anionic lipid accumulations and metabolism
    Analytical Chemistry, 2018
    Co-Authors: Wojciech Michno, Ibrahim Kaya, Sofie Nystrom, Laurent Guerard, Peter K R Nilsson, Per Hammarstrom, Kaj Blennow, Henrik Zetterberg
    Abstract:

    Amyloid Plaque formation constitutes one of the main pathological hallmarks of Alzheimer’s disease (AD) and is suggested to be a critical factor driving disease pathogenesis. Interestingly, in patients that display Amyloid pathology but remain cognitively normal, Aβ deposits are predominantly of diffuse morphology suggesting that cored Plaque formation is primarily associated with cognitive deterioration and AD pathogenesis. Little is known about the molecular mechanism responsible for conversion of monomeric Aβ into neurotoxic aggregates and the predominantly cored deposits observed in AD. The structural diversity among Aβ Plaques, including cored/compact- and diffuse, may be linked to their distinct Aβ profile and other chemical species including neuronal lipids. We developed a novel, chemical imaging paradigm combining matrix assisted laser desorption/ionization imaging mass spectrometry (MALDI IMS) and fluorescent Amyloid staining. This multimodal imaging approach was used to probe the lipid chemistry...

Thomas Enzlein - One of the best experts on this subject based on the ideXlab platform.

  • computational analysis of alzheimer Amyloid Plaque composition in 2d and elastically reconstructed 3d maldi ms images
    Analytical Chemistry, 2020
    Co-Authors: Wojciech Michno, Thomas Enzlein, Jonas Cordes, Bogdan Munteanu, Lutgarde Serneels, Bart De Strooper, Jorg Hanrieder
    Abstract:

    MALDI mass spectrometry imaging (MSI) enables label-free, spatially resolved analysis of a wide range of analytes in tissue sections. Quantitative analysis of MSI datasets is typically performed on single pixels or manually assigned regions of interest (ROIs). However, many sparse, small objects such as Alzheimer's disease (AD) brain deposits of Amyloid peptides called Plaques are neither single pixels nor ROIs. Here, we propose a new approach to facilitate the comparative computational evaluation of Amyloid Plaque-like objects by MSI: a fast Plaque PICKER tool that enables a statistical evaluation of heterogeneous Amyloid peptide composition. Comparing two AD mouse models, APP NL-G-F and APP PS1, we identified distinct heterogeneous Plaque populations in the NL-G-F model but only one class of Plaques in the PS1 model. We propose quantitative metrics for the comparison of technical and biological MSI replicates. Furthermore, we reconstructed a high-accuracy 3D-model of Amyloid Plaques in a fully automated fashion, employing rigid and elastic MSI image registration using structured and Plaque-unrelated reference ion images. Statistical single-Plaque analysis in reconstructed 3D-MSI objects revealed the Aβ1-42Arc peptide to be located either in the core of larger Plaques or in small Plaques without colocalization of other Aβ isoforms. In 3D, a substantially larger number of small Plaques were observed than that indicated by the 2D-MSI data, suggesting that quantitative analysis of molecularly diverse sparsely-distributed features may benefit from 3D-reconstruction. Data are available via ProteomeXchange with identifier PXD020824.