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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 : 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.

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  • 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.

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  • 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.

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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.

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  • 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.

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  • 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.

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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, 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.

    Free Register to Access Article

  • 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.

    Free Register to Access Article

  • 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.

    Free Register to Access Article