The Experts below are selected from a list of 342 Experts worldwide ranked by ideXlab platform

Karem H Alzoubi - One of the best experts on this subject based on the ideXlab platform.

  • arbutus andrachne l reverses sleep deprivation induced memory impairments in rats
    Molecular Neurobiology, 2018
    Co-Authors: Karem H Alzoubi, Omar F Khabour, Bayan S Malkawi, Tamam Elelimat, Feras Q Alali
    Abstract:

    Sleep deprivation (SD) is associated with cognitive deficits. It was found to affect the hippocampus region of the brain by impairing memory formation. This impairment is suggested to be caused by elevation in oxidative stress in the body, including the brain during SD. It was hypothesized that the methanolic extract of the fruits of Arbutus andrachne L. (Ericaceae) will prevent chronic SD-induced impairment of hippocampal memory via its antioxidative properties. The methanolic extract of the fruits of A. andrachne was evaluated for its beneficial properties to reverse SD-induced cognitive impairment in rats. Animals were sleep deprived for 8 weeks using a multiple Platform Model. The extract was administered i.p. at three doses (50, 200, and 500 mg/kg). Behavioral studies were conducted to test the spatial learning and memory using radial arm water maze (RAWM). In addition, the hippocampus was dissected to analyze the following oxidative stress markers: glutathione (GSH), oxidized glutathione (GSSG), GSH/GSSG, glutathione peroxidase (GPx), and catalase. Chronic SD impaired short- and long-term memories (P < 0.05). Treatment of animals with A. andrachne fruit extract at all doses prevented long-term memory impairment induced by SD while such treatment prevented short-term memory impairment only at 200 and 500 mg/kg dose levels. Moreover, A. andrachne fruit extract normalized the reduction in the hippocampus GSH/GSSG ratio and activity of GPx, and catalase (P < 0.05) induced by chronic sleep deprivation. Chronic sleep deprivation impaired both short- and long-term memory formation, while methanolic extract of A. andrachne fruits reversed this impairment, probably through normalizing oxidative stress in the hippocampus.

  • tempol prevents chronic sleep deprivation induced memory impairment
    Brain Research Bulletin, 2016
    Co-Authors: Karem H Alzoubi, Omar F Khabour, Amal S Albawaana, Farah H Alhashimi, Rabaa Y Athamneh
    Abstract:

    Sleep deprivation is associated with oxidative stress that causes learning and memory impairment. Tempol is a nitroxide compound that promotes the metabolism of many reactive oxygen species (ROS) and has antioxidant and neuroprotective effect. The current study investigated whether chronic administration of tempol can overcome oxidative stress and prevent learning and memory impairment induced by sleep deprivation. Sleep deprivation was induced in rats using multiple Platform Model. Tempol was administered to rats via oral gavages. Behavioral studies were conducted to test the spatial learning and memory using radial arm water maze. The hippocampus was dissected; antioxidant biomarkers (GSH, GSSG, GSH/GSSG ratio, GPx, SOD, and catalase) were assessed. The result of this project revealed that chronic sleep deprivation impaired both short and long term memory (P<0.05), while tempol treatment prevented such effect. Furthermore, tempol normalized chronic sleep deprivation induced reduction in the hippocampus activity of catalase, GPx, and SOD (P<0.05). Tempol also enhanced the ratio of GSH/GSSG in chronically sleep deprived rats treated with tempol as compared with only sleep deprived rats (P<0.05). In conclusion chronic sleep deprivation induced memory impairment, and treatment with tempol prevented this impairment probably through normalizing antioxidant mechanisms in the hippocampus.

  • the combined effect of sleep deprivation and western diet on spatial learning and memory role of bdnf and oxidative stress
    Journal of Molecular Neuroscience, 2013
    Co-Authors: Karem H Alzoubi, Omar F Khabour, Heba Salah, Baraa Abu E Rashid
    Abstract:

    Either sleep deprivation or Western diet can impair learning and memory via induction of oxidative stress, which results in neuronal damage and interference with the neurotransmission. In this study, we examined the combined effect of sleep deprivation and Western diet on hippocampus-dependent spatial learning and memory. In addition, possible molecular targets for sleep deprivation and Western diet-induced cognitive impairments were investigated. Sleep deprivation was induced in rats using the modified multiple Platform Model simultaneous with the administration of Western diet for 6 weeks. Thereafter, spatial learning and memory were tested using radial arm water maze. At the molecular level, BDNF protein and antioxidant markers including superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), glutathione (GSH), oxidized glutathione (GSSG), GSH/GSSG, and thiobarbituric acid reactive substances (TBARS) were assessed. The results of this study revealed that sleep deprivation, Western diet, or a combination of both impair short- and long-term memory (P < 0.05). The magnitude of the impairment induced by the combined treatment at the 24-h long-term memory was higher than that caused by each factor alone (P < 0.05). In addition, the combined treatment reduced the levels of hippocampal BDNF, a reduction that was not detected with each factor alone. Moreover, the combined treatment reduced the hippocampal activities of SOD, catalase, GPx, ratio of GSH/GSSG, and elevated TBARS level (P < 0.05). In conclusion, the combination of sleep deprivation and Western diet decreases BDNF levels and increases oxidative stress in the hippocampus, thus inducing memory impairment that is greater than the impairment produced by each factor alone.

  • the neuroprotective effect of vitamin e on chronic sleep deprivation induced memory impairment the role of oxidative stress
    Behavioural Brain Research, 2012
    Co-Authors: Karem H Alzoubi, Omar F Khabour, Baraa Abu E Rashid, Imad M Damaj, Heba Salah
    Abstract:

    Abstract Sleep deprivation induces oxidative stress and impairs learning and memory processes. Vitamin E, on the other hand, is a strong antioxidant that has neuroprotective effect on the brain. In this study, we examined the potential protective effect of chronic administration of vitamin E on chronic sleep deprivation-induced cognitive impairment. In addition, possible molecular targets for vitamin E effects on chronic sleep deprivation-induced cognitive impairment were determined. Sleep deprivation was induced in rats using modified multiple Platform Model. Vitamin E (100 mg/kg) was administered to animals by oral gavage. Behavioral study was conducted to test the spatial learning and memory using the radial arm water maze (RAWM). In addition, the hippocampus was dissected out and antioxidant markers including glutathione (GSH), oxidized glutathione (GSSG) and GSH/GSSG, glutathione peroxidase (GPx), catalase, and superoxide dismutase (SOD) were assessed. The results of this project revealed that chronic sleep deprivation impaired both (short- and long-term) memories (P

Omar F Khabour - One of the best experts on this subject based on the ideXlab platform.

  • arbutus andrachne l reverses sleep deprivation induced memory impairments in rats
    Molecular Neurobiology, 2018
    Co-Authors: Karem H Alzoubi, Omar F Khabour, Bayan S Malkawi, Tamam Elelimat, Feras Q Alali
    Abstract:

    Sleep deprivation (SD) is associated with cognitive deficits. It was found to affect the hippocampus region of the brain by impairing memory formation. This impairment is suggested to be caused by elevation in oxidative stress in the body, including the brain during SD. It was hypothesized that the methanolic extract of the fruits of Arbutus andrachne L. (Ericaceae) will prevent chronic SD-induced impairment of hippocampal memory via its antioxidative properties. The methanolic extract of the fruits of A. andrachne was evaluated for its beneficial properties to reverse SD-induced cognitive impairment in rats. Animals were sleep deprived for 8 weeks using a multiple Platform Model. The extract was administered i.p. at three doses (50, 200, and 500 mg/kg). Behavioral studies were conducted to test the spatial learning and memory using radial arm water maze (RAWM). In addition, the hippocampus was dissected to analyze the following oxidative stress markers: glutathione (GSH), oxidized glutathione (GSSG), GSH/GSSG, glutathione peroxidase (GPx), and catalase. Chronic SD impaired short- and long-term memories (P < 0.05). Treatment of animals with A. andrachne fruit extract at all doses prevented long-term memory impairment induced by SD while such treatment prevented short-term memory impairment only at 200 and 500 mg/kg dose levels. Moreover, A. andrachne fruit extract normalized the reduction in the hippocampus GSH/GSSG ratio and activity of GPx, and catalase (P < 0.05) induced by chronic sleep deprivation. Chronic sleep deprivation impaired both short- and long-term memory formation, while methanolic extract of A. andrachne fruits reversed this impairment, probably through normalizing oxidative stress in the hippocampus.

  • tempol prevents chronic sleep deprivation induced memory impairment
    Brain Research Bulletin, 2016
    Co-Authors: Karem H Alzoubi, Omar F Khabour, Amal S Albawaana, Farah H Alhashimi, Rabaa Y Athamneh
    Abstract:

    Sleep deprivation is associated with oxidative stress that causes learning and memory impairment. Tempol is a nitroxide compound that promotes the metabolism of many reactive oxygen species (ROS) and has antioxidant and neuroprotective effect. The current study investigated whether chronic administration of tempol can overcome oxidative stress and prevent learning and memory impairment induced by sleep deprivation. Sleep deprivation was induced in rats using multiple Platform Model. Tempol was administered to rats via oral gavages. Behavioral studies were conducted to test the spatial learning and memory using radial arm water maze. The hippocampus was dissected; antioxidant biomarkers (GSH, GSSG, GSH/GSSG ratio, GPx, SOD, and catalase) were assessed. The result of this project revealed that chronic sleep deprivation impaired both short and long term memory (P<0.05), while tempol treatment prevented such effect. Furthermore, tempol normalized chronic sleep deprivation induced reduction in the hippocampus activity of catalase, GPx, and SOD (P<0.05). Tempol also enhanced the ratio of GSH/GSSG in chronically sleep deprived rats treated with tempol as compared with only sleep deprived rats (P<0.05). In conclusion chronic sleep deprivation induced memory impairment, and treatment with tempol prevented this impairment probably through normalizing antioxidant mechanisms in the hippocampus.

  • the combined effect of sleep deprivation and western diet on spatial learning and memory role of bdnf and oxidative stress
    Journal of Molecular Neuroscience, 2013
    Co-Authors: Karem H Alzoubi, Omar F Khabour, Heba Salah, Baraa Abu E Rashid
    Abstract:

    Either sleep deprivation or Western diet can impair learning and memory via induction of oxidative stress, which results in neuronal damage and interference with the neurotransmission. In this study, we examined the combined effect of sleep deprivation and Western diet on hippocampus-dependent spatial learning and memory. In addition, possible molecular targets for sleep deprivation and Western diet-induced cognitive impairments were investigated. Sleep deprivation was induced in rats using the modified multiple Platform Model simultaneous with the administration of Western diet for 6 weeks. Thereafter, spatial learning and memory were tested using radial arm water maze. At the molecular level, BDNF protein and antioxidant markers including superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), glutathione (GSH), oxidized glutathione (GSSG), GSH/GSSG, and thiobarbituric acid reactive substances (TBARS) were assessed. The results of this study revealed that sleep deprivation, Western diet, or a combination of both impair short- and long-term memory (P < 0.05). The magnitude of the impairment induced by the combined treatment at the 24-h long-term memory was higher than that caused by each factor alone (P < 0.05). In addition, the combined treatment reduced the levels of hippocampal BDNF, a reduction that was not detected with each factor alone. Moreover, the combined treatment reduced the hippocampal activities of SOD, catalase, GPx, ratio of GSH/GSSG, and elevated TBARS level (P < 0.05). In conclusion, the combination of sleep deprivation and Western diet decreases BDNF levels and increases oxidative stress in the hippocampus, thus inducing memory impairment that is greater than the impairment produced by each factor alone.

  • the neuroprotective effect of vitamin e on chronic sleep deprivation induced memory impairment the role of oxidative stress
    Behavioural Brain Research, 2012
    Co-Authors: Karem H Alzoubi, Omar F Khabour, Baraa Abu E Rashid, Imad M Damaj, Heba Salah
    Abstract:

    Abstract Sleep deprivation induces oxidative stress and impairs learning and memory processes. Vitamin E, on the other hand, is a strong antioxidant that has neuroprotective effect on the brain. In this study, we examined the potential protective effect of chronic administration of vitamin E on chronic sleep deprivation-induced cognitive impairment. In addition, possible molecular targets for vitamin E effects on chronic sleep deprivation-induced cognitive impairment were determined. Sleep deprivation was induced in rats using modified multiple Platform Model. Vitamin E (100 mg/kg) was administered to animals by oral gavage. Behavioral study was conducted to test the spatial learning and memory using the radial arm water maze (RAWM). In addition, the hippocampus was dissected out and antioxidant markers including glutathione (GSH), oxidized glutathione (GSSG) and GSH/GSSG, glutathione peroxidase (GPx), catalase, and superoxide dismutase (SOD) were assessed. The results of this project revealed that chronic sleep deprivation impaired both (short- and long-term) memories (P

Heba Salah - One of the best experts on this subject based on the ideXlab platform.

  • the combined effect of sleep deprivation and western diet on spatial learning and memory role of bdnf and oxidative stress
    Journal of Molecular Neuroscience, 2013
    Co-Authors: Karem H Alzoubi, Omar F Khabour, Heba Salah, Baraa Abu E Rashid
    Abstract:

    Either sleep deprivation or Western diet can impair learning and memory via induction of oxidative stress, which results in neuronal damage and interference with the neurotransmission. In this study, we examined the combined effect of sleep deprivation and Western diet on hippocampus-dependent spatial learning and memory. In addition, possible molecular targets for sleep deprivation and Western diet-induced cognitive impairments were investigated. Sleep deprivation was induced in rats using the modified multiple Platform Model simultaneous with the administration of Western diet for 6 weeks. Thereafter, spatial learning and memory were tested using radial arm water maze. At the molecular level, BDNF protein and antioxidant markers including superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), glutathione (GSH), oxidized glutathione (GSSG), GSH/GSSG, and thiobarbituric acid reactive substances (TBARS) were assessed. The results of this study revealed that sleep deprivation, Western diet, or a combination of both impair short- and long-term memory (P < 0.05). The magnitude of the impairment induced by the combined treatment at the 24-h long-term memory was higher than that caused by each factor alone (P < 0.05). In addition, the combined treatment reduced the levels of hippocampal BDNF, a reduction that was not detected with each factor alone. Moreover, the combined treatment reduced the hippocampal activities of SOD, catalase, GPx, ratio of GSH/GSSG, and elevated TBARS level (P < 0.05). In conclusion, the combination of sleep deprivation and Western diet decreases BDNF levels and increases oxidative stress in the hippocampus, thus inducing memory impairment that is greater than the impairment produced by each factor alone.

  • the neuroprotective effect of vitamin e on chronic sleep deprivation induced memory impairment the role of oxidative stress
    Behavioural Brain Research, 2012
    Co-Authors: Karem H Alzoubi, Omar F Khabour, Baraa Abu E Rashid, Imad M Damaj, Heba Salah
    Abstract:

    Abstract Sleep deprivation induces oxidative stress and impairs learning and memory processes. Vitamin E, on the other hand, is a strong antioxidant that has neuroprotective effect on the brain. In this study, we examined the potential protective effect of chronic administration of vitamin E on chronic sleep deprivation-induced cognitive impairment. In addition, possible molecular targets for vitamin E effects on chronic sleep deprivation-induced cognitive impairment were determined. Sleep deprivation was induced in rats using modified multiple Platform Model. Vitamin E (100 mg/kg) was administered to animals by oral gavage. Behavioral study was conducted to test the spatial learning and memory using the radial arm water maze (RAWM). In addition, the hippocampus was dissected out and antioxidant markers including glutathione (GSH), oxidized glutathione (GSSG) and GSH/GSSG, glutathione peroxidase (GPx), catalase, and superoxide dismutase (SOD) were assessed. The results of this project revealed that chronic sleep deprivation impaired both (short- and long-term) memories (P

Baraa Abu E Rashid - One of the best experts on this subject based on the ideXlab platform.

  • the combined effect of sleep deprivation and western diet on spatial learning and memory role of bdnf and oxidative stress
    Journal of Molecular Neuroscience, 2013
    Co-Authors: Karem H Alzoubi, Omar F Khabour, Heba Salah, Baraa Abu E Rashid
    Abstract:

    Either sleep deprivation or Western diet can impair learning and memory via induction of oxidative stress, which results in neuronal damage and interference with the neurotransmission. In this study, we examined the combined effect of sleep deprivation and Western diet on hippocampus-dependent spatial learning and memory. In addition, possible molecular targets for sleep deprivation and Western diet-induced cognitive impairments were investigated. Sleep deprivation was induced in rats using the modified multiple Platform Model simultaneous with the administration of Western diet for 6 weeks. Thereafter, spatial learning and memory were tested using radial arm water maze. At the molecular level, BDNF protein and antioxidant markers including superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), glutathione (GSH), oxidized glutathione (GSSG), GSH/GSSG, and thiobarbituric acid reactive substances (TBARS) were assessed. The results of this study revealed that sleep deprivation, Western diet, or a combination of both impair short- and long-term memory (P < 0.05). The magnitude of the impairment induced by the combined treatment at the 24-h long-term memory was higher than that caused by each factor alone (P < 0.05). In addition, the combined treatment reduced the levels of hippocampal BDNF, a reduction that was not detected with each factor alone. Moreover, the combined treatment reduced the hippocampal activities of SOD, catalase, GPx, ratio of GSH/GSSG, and elevated TBARS level (P < 0.05). In conclusion, the combination of sleep deprivation and Western diet decreases BDNF levels and increases oxidative stress in the hippocampus, thus inducing memory impairment that is greater than the impairment produced by each factor alone.

  • the neuroprotective effect of vitamin e on chronic sleep deprivation induced memory impairment the role of oxidative stress
    Behavioural Brain Research, 2012
    Co-Authors: Karem H Alzoubi, Omar F Khabour, Baraa Abu E Rashid, Imad M Damaj, Heba Salah
    Abstract:

    Abstract Sleep deprivation induces oxidative stress and impairs learning and memory processes. Vitamin E, on the other hand, is a strong antioxidant that has neuroprotective effect on the brain. In this study, we examined the potential protective effect of chronic administration of vitamin E on chronic sleep deprivation-induced cognitive impairment. In addition, possible molecular targets for vitamin E effects on chronic sleep deprivation-induced cognitive impairment were determined. Sleep deprivation was induced in rats using modified multiple Platform Model. Vitamin E (100 mg/kg) was administered to animals by oral gavage. Behavioral study was conducted to test the spatial learning and memory using the radial arm water maze (RAWM). In addition, the hippocampus was dissected out and antioxidant markers including glutathione (GSH), oxidized glutathione (GSSG) and GSH/GSSG, glutathione peroxidase (GPx), catalase, and superoxide dismutase (SOD) were assessed. The results of this project revealed that chronic sleep deprivation impaired both (short- and long-term) memories (P

Rabaa Y Athamneh - One of the best experts on this subject based on the ideXlab platform.

  • tempol prevents chronic sleep deprivation induced memory impairment
    Brain Research Bulletin, 2016
    Co-Authors: Karem H Alzoubi, Omar F Khabour, Amal S Albawaana, Farah H Alhashimi, Rabaa Y Athamneh
    Abstract:

    Sleep deprivation is associated with oxidative stress that causes learning and memory impairment. Tempol is a nitroxide compound that promotes the metabolism of many reactive oxygen species (ROS) and has antioxidant and neuroprotective effect. The current study investigated whether chronic administration of tempol can overcome oxidative stress and prevent learning and memory impairment induced by sleep deprivation. Sleep deprivation was induced in rats using multiple Platform Model. Tempol was administered to rats via oral gavages. Behavioral studies were conducted to test the spatial learning and memory using radial arm water maze. The hippocampus was dissected; antioxidant biomarkers (GSH, GSSG, GSH/GSSG ratio, GPx, SOD, and catalase) were assessed. The result of this project revealed that chronic sleep deprivation impaired both short and long term memory (P<0.05), while tempol treatment prevented such effect. Furthermore, tempol normalized chronic sleep deprivation induced reduction in the hippocampus activity of catalase, GPx, and SOD (P<0.05). Tempol also enhanced the ratio of GSH/GSSG in chronically sleep deprived rats treated with tempol as compared with only sleep deprived rats (P<0.05). In conclusion chronic sleep deprivation induced memory impairment, and treatment with tempol prevented this impairment probably through normalizing antioxidant mechanisms in the hippocampus.