The Experts below are selected from a list of 15 Experts worldwide ranked by ideXlab platform

Jacques Hugon - One of the best experts on this subject based on the ideXlab platform.

  • Dose-dependent neuroprotective effect of the JNK inhibitor Brimapitide in 5xFAD transgenic mice.
    Brain Research, 2020
    Co-Authors: Baptiste Porte, Gwendolyn Marguerit, Sylvie Thomasseau, Claire Paquet, Jacques Hugon
    Abstract:

    Abstract Alzheimer’s disease (AD) is a neurodegenerative disease mainly affecting old people. According to the “amyloid cascade hypothesis”, the accumulation of Aβ oligomers could lead to kinase activation and Tau phosphorylation. Activated kinases include c-Jun N-terminal kinase (JNK) and previous studies highlighted the beneficial effects of the JNK-specific inhibitor Brimapitide (10 mg/kg) in 5xFAD transgenic mice. Our aim was to evaluate the effects of decreasing doses of Brimapitide on cognition and neurodegeneration in early treated 5xFAD mice. Three month-old 5xFAD were intravenously treated for 6 months with either Brimapitide (3 mg/kg or 0.3 mg/kg) or Nacl. Cognition and amyloid burden, neuronal and synaptic impairments were evaluated. Low doses of Brimapitide (0.3 mg/kg) reduced neuronal degeneration and improved cognition in treated mice compared to non-treated mice. Amyloid burden and synaptic degeneration only decreased with the 3 mg/kg dose. This JNK inhibitor can afford neuroprotection but with a differential effect on amyloid deposition in 5xFAD mice. Brimapitide might partially prevent ongoing neurodegeneration in 5xFAD mice.

  • Brimapitide Reduced Neuronal Stress Markers and Cognitive Deficits in 5XFAD Transgenic Mice.
    Journal of Alzheimer's Disease, 2018
    Co-Authors: Sarah Gourmaud, Sylvie Thomasseau, Claire Paquet, Priscilla Thomas, Marion Tible, Claire Abadie, Jacques Hugon
    Abstract:

    Alzheimer's disease (AD) is characterized by accumulations of amyloid-β (Aβ42) and hyperphosphorylated tau proteins, associated with neuroinflammation, synaptic loss, and neuronal death. Several studies indicate that c-Jun N-terminal kinase (JNK) is implicated in the pathological features of AD. We have investigated in 5XFAD mice, the therapeutic effects of Brimapitide, a JNK-specific inhibitory peptide previously tested with higher concentrations in another AD model (TgCRND8). Three-month-old 5XFAD and wild-type littermate mice were treated by intravenous injections of low doses (10 mg/kg) of Brimapitide every 3 weeks, for 3 or 6 months (n = 6-9 per group). Cognitive deficits and brain lesions were assessed using Y-maze, fear-conditioning test, and histological and biochemical methods. Chronic treatment of Brimapitide for 3 months resulted in a reduction of Aβ plaque burden in the cortex of 5XFAD treated mice. After 6 months of treatment, cognitive deficits were reduced but also a significant reduction of cell death markers and the pro-inflammatory IL-1β cytokine in treated mice were detected. The Aβ plaque burden was not anymore modified by the 6 months of treatment. In addition to modulating cognition and amyloid plaque accumulation, depending on the treatment duration, Brimapitide seems experimentally to reduce neuronal stress in 5XFAD mice.

Sylvie Thomasseau - One of the best experts on this subject based on the ideXlab platform.

  • Dose-dependent neuroprotective effect of the JNK inhibitor Brimapitide in 5xFAD transgenic mice.
    Brain Research, 2020
    Co-Authors: Baptiste Porte, Gwendolyn Marguerit, Sylvie Thomasseau, Claire Paquet, Jacques Hugon
    Abstract:

    Abstract Alzheimer’s disease (AD) is a neurodegenerative disease mainly affecting old people. According to the “amyloid cascade hypothesis”, the accumulation of Aβ oligomers could lead to kinase activation and Tau phosphorylation. Activated kinases include c-Jun N-terminal kinase (JNK) and previous studies highlighted the beneficial effects of the JNK-specific inhibitor Brimapitide (10 mg/kg) in 5xFAD transgenic mice. Our aim was to evaluate the effects of decreasing doses of Brimapitide on cognition and neurodegeneration in early treated 5xFAD mice. Three month-old 5xFAD were intravenously treated for 6 months with either Brimapitide (3 mg/kg or 0.3 mg/kg) or Nacl. Cognition and amyloid burden, neuronal and synaptic impairments were evaluated. Low doses of Brimapitide (0.3 mg/kg) reduced neuronal degeneration and improved cognition in treated mice compared to non-treated mice. Amyloid burden and synaptic degeneration only decreased with the 3 mg/kg dose. This JNK inhibitor can afford neuroprotection but with a differential effect on amyloid deposition in 5xFAD mice. Brimapitide might partially prevent ongoing neurodegeneration in 5xFAD mice.

  • Brimapitide Reduced Neuronal Stress Markers and Cognitive Deficits in 5XFAD Transgenic Mice.
    Journal of Alzheimer's Disease, 2018
    Co-Authors: Sarah Gourmaud, Sylvie Thomasseau, Claire Paquet, Priscilla Thomas, Marion Tible, Claire Abadie, Jacques Hugon
    Abstract:

    Alzheimer's disease (AD) is characterized by accumulations of amyloid-β (Aβ42) and hyperphosphorylated tau proteins, associated with neuroinflammation, synaptic loss, and neuronal death. Several studies indicate that c-Jun N-terminal kinase (JNK) is implicated in the pathological features of AD. We have investigated in 5XFAD mice, the therapeutic effects of Brimapitide, a JNK-specific inhibitory peptide previously tested with higher concentrations in another AD model (TgCRND8). Three-month-old 5XFAD and wild-type littermate mice were treated by intravenous injections of low doses (10 mg/kg) of Brimapitide every 3 weeks, for 3 or 6 months (n = 6-9 per group). Cognitive deficits and brain lesions were assessed using Y-maze, fear-conditioning test, and histological and biochemical methods. Chronic treatment of Brimapitide for 3 months resulted in a reduction of Aβ plaque burden in the cortex of 5XFAD treated mice. After 6 months of treatment, cognitive deficits were reduced but also a significant reduction of cell death markers and the pro-inflammatory IL-1β cytokine in treated mice were detected. The Aβ plaque burden was not anymore modified by the 6 months of treatment. In addition to modulating cognition and amyloid plaque accumulation, depending on the treatment duration, Brimapitide seems experimentally to reduce neuronal stress in 5XFAD mice.

Claire Paquet - One of the best experts on this subject based on the ideXlab platform.

  • Dose-dependent neuroprotective effect of the JNK inhibitor Brimapitide in 5xFAD transgenic mice.
    Brain Research, 2020
    Co-Authors: Baptiste Porte, Gwendolyn Marguerit, Sylvie Thomasseau, Claire Paquet, Jacques Hugon
    Abstract:

    Abstract Alzheimer’s disease (AD) is a neurodegenerative disease mainly affecting old people. According to the “amyloid cascade hypothesis”, the accumulation of Aβ oligomers could lead to kinase activation and Tau phosphorylation. Activated kinases include c-Jun N-terminal kinase (JNK) and previous studies highlighted the beneficial effects of the JNK-specific inhibitor Brimapitide (10 mg/kg) in 5xFAD transgenic mice. Our aim was to evaluate the effects of decreasing doses of Brimapitide on cognition and neurodegeneration in early treated 5xFAD mice. Three month-old 5xFAD were intravenously treated for 6 months with either Brimapitide (3 mg/kg or 0.3 mg/kg) or Nacl. Cognition and amyloid burden, neuronal and synaptic impairments were evaluated. Low doses of Brimapitide (0.3 mg/kg) reduced neuronal degeneration and improved cognition in treated mice compared to non-treated mice. Amyloid burden and synaptic degeneration only decreased with the 3 mg/kg dose. This JNK inhibitor can afford neuroprotection but with a differential effect on amyloid deposition in 5xFAD mice. Brimapitide might partially prevent ongoing neurodegeneration in 5xFAD mice.

  • Brimapitide Reduced Neuronal Stress Markers and Cognitive Deficits in 5XFAD Transgenic Mice.
    Journal of Alzheimer's Disease, 2018
    Co-Authors: Sarah Gourmaud, Sylvie Thomasseau, Claire Paquet, Priscilla Thomas, Marion Tible, Claire Abadie, Jacques Hugon
    Abstract:

    Alzheimer's disease (AD) is characterized by accumulations of amyloid-β (Aβ42) and hyperphosphorylated tau proteins, associated with neuroinflammation, synaptic loss, and neuronal death. Several studies indicate that c-Jun N-terminal kinase (JNK) is implicated in the pathological features of AD. We have investigated in 5XFAD mice, the therapeutic effects of Brimapitide, a JNK-specific inhibitory peptide previously tested with higher concentrations in another AD model (TgCRND8). Three-month-old 5XFAD and wild-type littermate mice were treated by intravenous injections of low doses (10 mg/kg) of Brimapitide every 3 weeks, for 3 or 6 months (n = 6-9 per group). Cognitive deficits and brain lesions were assessed using Y-maze, fear-conditioning test, and histological and biochemical methods. Chronic treatment of Brimapitide for 3 months resulted in a reduction of Aβ plaque burden in the cortex of 5XFAD treated mice. After 6 months of treatment, cognitive deficits were reduced but also a significant reduction of cell death markers and the pro-inflammatory IL-1β cytokine in treated mice were detected. The Aβ plaque burden was not anymore modified by the 6 months of treatment. In addition to modulating cognition and amyloid plaque accumulation, depending on the treatment duration, Brimapitide seems experimentally to reduce neuronal stress in 5XFAD mice.

Baptiste Porte - One of the best experts on this subject based on the ideXlab platform.

  • Dose-dependent neuroprotective effect of the JNK inhibitor Brimapitide in 5xFAD transgenic mice.
    Brain Research, 2020
    Co-Authors: Baptiste Porte, Gwendolyn Marguerit, Sylvie Thomasseau, Claire Paquet, Jacques Hugon
    Abstract:

    Abstract Alzheimer’s disease (AD) is a neurodegenerative disease mainly affecting old people. According to the “amyloid cascade hypothesis”, the accumulation of Aβ oligomers could lead to kinase activation and Tau phosphorylation. Activated kinases include c-Jun N-terminal kinase (JNK) and previous studies highlighted the beneficial effects of the JNK-specific inhibitor Brimapitide (10 mg/kg) in 5xFAD transgenic mice. Our aim was to evaluate the effects of decreasing doses of Brimapitide on cognition and neurodegeneration in early treated 5xFAD mice. Three month-old 5xFAD were intravenously treated for 6 months with either Brimapitide (3 mg/kg or 0.3 mg/kg) or Nacl. Cognition and amyloid burden, neuronal and synaptic impairments were evaluated. Low doses of Brimapitide (0.3 mg/kg) reduced neuronal degeneration and improved cognition in treated mice compared to non-treated mice. Amyloid burden and synaptic degeneration only decreased with the 3 mg/kg dose. This JNK inhibitor can afford neuroprotection but with a differential effect on amyloid deposition in 5xFAD mice. Brimapitide might partially prevent ongoing neurodegeneration in 5xFAD mice.

Gwendolyn Marguerit - One of the best experts on this subject based on the ideXlab platform.

  • Dose-dependent neuroprotective effect of the JNK inhibitor Brimapitide in 5xFAD transgenic mice.
    Brain Research, 2020
    Co-Authors: Baptiste Porte, Gwendolyn Marguerit, Sylvie Thomasseau, Claire Paquet, Jacques Hugon
    Abstract:

    Abstract Alzheimer’s disease (AD) is a neurodegenerative disease mainly affecting old people. According to the “amyloid cascade hypothesis”, the accumulation of Aβ oligomers could lead to kinase activation and Tau phosphorylation. Activated kinases include c-Jun N-terminal kinase (JNK) and previous studies highlighted the beneficial effects of the JNK-specific inhibitor Brimapitide (10 mg/kg) in 5xFAD transgenic mice. Our aim was to evaluate the effects of decreasing doses of Brimapitide on cognition and neurodegeneration in early treated 5xFAD mice. Three month-old 5xFAD were intravenously treated for 6 months with either Brimapitide (3 mg/kg or 0.3 mg/kg) or Nacl. Cognition and amyloid burden, neuronal and synaptic impairments were evaluated. Low doses of Brimapitide (0.3 mg/kg) reduced neuronal degeneration and improved cognition in treated mice compared to non-treated mice. Amyloid burden and synaptic degeneration only decreased with the 3 mg/kg dose. This JNK inhibitor can afford neuroprotection but with a differential effect on amyloid deposition in 5xFAD mice. Brimapitide might partially prevent ongoing neurodegeneration in 5xFAD mice.