The Experts below are selected from a list of 18948 Experts worldwide ranked by ideXlab platform

Richard S Jope - One of the best experts on this subject based on the ideXlab platform.

  • Glycogen Synthase Kinase 3 gsk3 regulation actions and diseases
    Pharmacology & Therapeutics, 2015
    Co-Authors: Eleonore Beurel, Steven F Grieco, Richard S Jope
    Abstract:

    Glycogen Synthase Kinase-3 (GSK3) may be the busiest Kinase in most cells, with over 100 known substrates to deal with. How does GSK3 maintain control to selectively phosphorylate each substrate, and why was it evolutionarily favorable for GSK3 to assume such a large responsibility? GSK3 must be particularly adaptable for incorporating new substrates into its repertoire, and we discuss the distinct properties of GSK3 that may contribute to its capacity to fulfill its roles in multiple signaling pathways. The mechanisms regulating GSK3 (predominantly post-translational modifications, substrate priming, cellular trafficking, protein complexes) have been reviewed previously, so here we focus on newly identified complexities in these mechanisms, how each of these regulatory mechanism contributes to the ability of GSK3 to select which substrates to phosphorylate, and how these mechanisms may have contributed to its adaptability as new substrates evolved. The current understanding of the mechanisms regulating GSK3 is reviewed, as are emerging topics in the actions of GSK3, particularly its interactions with receptors and receptor-coupled signal transduction events, and differential actions and regulation of the two GSK3 isoforms, GSK3α and GSK3β. Another remarkable characteristic of GSK3 is its involvement in many prevalent disorders, including psychiatric and neurological diseases, inflammatory diseases, cancer, and others. We address the feasibility of targeting GSK3 therapeutically, and provide an update of its involvement in the etiology and treatment of several disorders.

  • Glycogen Synthase Kinase 3 inhibitors rescuers of cognitive impairments
    Pharmacology & Therapeutics, 2014
    Co-Authors: Margaret K King, Richard S Jope, Marta Pardo, Yuyan Cheng, Kimberlee Downey, Eleonore Beurel
    Abstract:

    Impairment of cognitive processes is a devastating outcome of many diseases, injuries, and drugs affecting the central nervous system (CNS). Most often, very little can be done by available therapeutic interventions to improve cognitive functions. Here we review evidence that inhibition of Glycogen Synthase Kinase-3 (GSK3) ameliorates cognitive deficits in a wide variety of animal models of CNS diseases, including Alzheimer's disease, Fragile X syndrome, Down syndrome, Parkinson's disease, spinocerebellar ataxia type 1, traumatic brain injury, and others. GSK3 inhibitors also improve cognition following impairments caused by therapeutic interventions, such as cranial irradiation for brain tumors. These findings demonstrate that GSK3 inhibitors are able to ameliorate cognitive impairments caused by a diverse array of diseases, injury, and treatments. The improvements in impaired cognition instilled by administration of GSK3 inhibitors appear to involve a variety of different mechanisms, such as supporting long-term potentiation and diminishing long-term depression, promotion of neurogenesis, reduction of inflammation, and increasing a number of neuroprotective mechanisms. The potential for GSK3 inhibitors to repair cognitive deficits associated with many conditions warrants further investigation of their potential for therapeutic interventions, particularly considering the current dearth of treatments available to reduce loss of cognitive functions.

  • inhibition of Glycogen Synthase Kinase 3 is necessary for the rapid antidepressant effect of ketamine in mice
    Molecular Psychiatry, 2011
    Co-Authors: Eleonore Beurel, Ling Song, Richard S Jope
    Abstract:

    Inhibition of Glycogen Synthase Kinase-3 is necessary for the rapid antidepressant effect of ketamine in mice

  • innate and adaptive immune responses regulated by Glycogen Synthase Kinase 3 gsk3
    Trends in Immunology, 2010
    Co-Authors: Eleonore Beurel, Suzanne M Michalek, Richard S Jope
    Abstract:

    In just a few years, the view of Glycogen Synthase Kinase-3 (GSK3) has been transformed from an obscure enzyme seldom encountered in the immune literature to one implicated in an improbably large number of roles. GSK3 is a crucial regulator of the balance between pro- and anti-inflammatory cytokine production in both the periphery and the central nervous system, so that GSK3 inhibitors such as lithium can diminish inflammation. GSK3 influences T-cell proliferation, differentiation and survival. Many effects stem from GSK3 regulation of critical transcription factors, such as NF-κB, NFAT and STATs. These discoveries led to the rapid application of GSK3 inhibitors to animal models of sepsis, arthritis, colitis, multiple sclerosis and others, demonstrating their potential for therapeutic intervention.

  • Glycogen Synthase Kinase 3 gsk3 inflammation diseases and therapeutics
    Neurochemical Research, 2007
    Co-Authors: Richard S Jope, Christopher J Yuskaitis, Eleonore Beurel
    Abstract:

    Deciphering what governs inflammation and its effects on tissues is vital for understanding many pathologies. The recent discovery that Glycogen Synthase Kinase-3 (GSK3) promotes inflammation reveals a new component of its well-documented actions in several prevalent diseases which involve inflammation, including mood disorders, Alzheimer’s disease, diabetes, and cancer. Involvement in such disparate conditions stems from the widespread influences of GSK3 on many cellular functions, with this review focusing on its regulation of inflammatory processes. GSK3 promotes the production of inflammatory molecules and cell migration, which together make GSK3 a powerful regulator of inflammation, while GSK3 inhibition provides protection from inflammatory conditions in animal models. The involvement of GSK3 and inflammation in these diseases are highlighted. Thus, GSK3 may contribute not only to primary pathologies in these diseases, but also to the associated inflammation, suggesting that GSK3 inhibitors may have multiple effects influencing these conditions.

William H. Gerwick - One of the best experts on this subject based on the ideXlab platform.

  • eckmaxol a phlorotannin extracted from ecklonia maxima produces anti β amyloid oligomer neuroprotective effects possibly via directly acting on Glycogen Synthase Kinase 3β
    ACS Chemical Neuroscience, 2018
    Co-Authors: Jialing Wang, Jiachen Zheng, Chunhui Huang, Jiaying Zhao, Jiajia Lin, Xuezhen Zhou, Benjamin C. Naman, Ning Wang, William H. Gerwick
    Abstract:

    Alzheimer’s disease is a progressive neurodegenerative disorder that mainly affects the elderly. Soluble β-amyloid oligomer, which can induce neurotoxicity, is generally regarded as the main neurotoxin in Alzheimer’s disease. Here we report that eckmaxol, a phlorotannin extracted from the brown alga Ecklonia maxima, could produce neuroprotective effects in SH-SY5Y cells. Eckmaxol effectively prevented but did not rescue β-amyloid oligomer-induced neuronal apoptosis and increase of intracellular reactive oxygen species. Eckmaxol also significantly reversed the decreased expression of phospho-Ser9-Glycogen Synthase Kinase 3β and increased expression of phospho-extracellular signal-regulated Kinase, which was induced by Aβ oligomer. Moreover, both Glycogen Synthase Kinase 3β and mitogen activated protein Kinase inhibitors produced neuroprotective effects in SH-SY5Y cells. Furthermore, eckmaxol showed favorable interaction in the ATP binding site of Glycogen Synthase Kinase 3β and mitogen activated protein ki...

  • Eckmaxol, a Phlorotannin Extracted from Ecklonia maxima, Produces Anti-β-amyloid Oligomer Neuroprotective Effects Possibly via Directly Acting on Glycogen Synthase Kinase 3β
    2018
    Co-Authors: Jialing Wang, Jiachen Zheng, Chunhui Huang, Jiaying Zhao, Jiajia Lin, Xuezhen Zhou, Benjamin C. Naman, Ning Wang, William H. Gerwick, Qinwen Wang
    Abstract:

    Alzheimer’s disease is a progressive neurodegenerative disorder that mainly affects the elderly. Soluble β-amyloid oligomer, which can induce neurotoxicity, is generally regarded as the main neurotoxin in Alzheimer’s disease. Here we report that eckmaxol, a phlorotannin extracted from the brown alga Ecklonia maxima, could produce neuroprotective effects in SH-SY5Y cells. Eckmaxol effectively prevented but did not rescue β-amyloid oligomer-induced neuronal apoptosis and increase of intracellular reactive oxygen species. Eckmaxol also significantly reversed the decreased expression of phospho-Ser9-Glycogen Synthase Kinase 3β and increased expression of phospho-extracellular signal-regulated Kinase, which was induced by Aβ oligomer. Moreover, both Glycogen Synthase Kinase 3β and mitogen activated protein Kinase inhibitors produced neuroprotective effects in SH-SY5Y cells. Furthermore, eckmaxol showed favorable interaction in the ATP binding site of Glycogen Synthase Kinase 3β and mitogen activated protein Kinase. These results suggested that eckmaxol might produce neuroprotective effects via concurrent inhibition of Glycogen Synthase Kinase 3β and extracellular signal-regulated Kinase pathways, possibly via directly acting on Glycogen Synthase Kinase 3β and mitogen activated protein Kinase. Based on the central role that β-amyloid oligomers play in the pathogenesis of Alzheimer’s disease and the high annual production of Ecklonia maxima for alginate and other nutritional ingredients, this report represents a new candidate for the treatment of Alzheimer’s disease, and also expands the potential application of Ecklonia maxima and its constituents in the field of pharmacology

James R Woodgett - One of the best experts on this subject based on the ideXlab platform.

  • cardiac fibroblast Glycogen Synthase Kinase 3β regulates ventricular remodeling and dysfunction in ischemic heart
    Circulation, 2014
    Co-Authors: Firdos Ahmad, James R Woodgett, Jibin Zhou, Justine E Yu, Ronald J Vagnozzi, Daohai Yu, Emily J Tsai, Thomas Force
    Abstract:

    Background—Myocardial infarction–induced remodeling includes chamber dilatation, contractile dysfunction, and fibrosis. Of these, fibrosis is the least understood. After myocardial infarction, activated cardiac fibroblasts deposit extracellular matrix. Current therapies to prevent fibrosis are inadequate, and new molecular targets are needed. Methods and Results—Herein we report that Glycogen Synthase Kinase-3β (GSK-3β) is phosphorylated (inhibited) in fibrotic tissues from ischemic human and mouse heart. Using 2 fibroblast-specific GSK-3β knockout mouse models, we show that deletion of GSK-3β in cardiac fibroblasts leads to fibrogenesis, left ventricular dysfunction, and excessive scarring in the ischemic heart. Deletion of GSK-3β induces a profibrotic myofibroblast phenotype in isolated cardiac fibroblasts, in post–myocardial infarction hearts, and in mouse embryonic fibroblasts deleted for GSK-3β. Mechanistically, GSK-3β inhibits profibrotic transforming growth factor-β1/SMAD-3 signaling via interactio...

  • tissue specific role of Glycogen Synthase Kinase 3β in glucose homeostasis and insulin action
    Molecular and Cellular Biology, 2008
    Co-Authors: Satish Patel, Bradley W Doble, Katrina Macaulay, Elaine M Sinclair, Daniel J Drucker, James R Woodgett
    Abstract:

    Dysregulation of the protein Kinase Glycogen Synthase Kinase 3 (GSK-3) has been implicated in the development of type 2 diabetes mellitus. GSK-3 protein expression and Kinase activity are elevated in diabetes, while selective GSK-3 inhibitors have shown promise as modulators of glucose metabolism and insulin sensitivity. There are two GSK-3 isoforms in mammals, GSK-3 and GSK-3. Mice engineered to lack GSK-3 die in late embryogenesis from liver apoptosis, whereas mice engineered to lack GSK-3 are viable and exhibit improved insulin sensitivity and hepatic glucose homeostasis. To assess the potential role of GSK-3 in insulin function, a conditional gene-targeting approach whereby mice in which expression of GSK-3 was specifically ablated within insulin-sensitive tissues were generated was undertaken. Liver-specific GSK-3 knockout mice are viable and glucose and insulin tolerant and display “normal” metabolic characteristics and insulin signaling. Mice lacking expression of GSK-3 in skeletal muscle are also viable but, in contrast to the liver-deleted animals, display improved glucose tolerance that is coupled with enhanced insulin-stimulated Glycogen Synthase regulation and Glycogen deposition. These data indicate that there are not only distinct roles for GSK-3 and GSK-3 within the adult but also tissue-specific phenotypes associated with each of these isoforms. Glycogen Synthase Kinase 3 (GSK-3) is a highly conserved, ubiquitously expressed serine/threonine protein Kinase that exists as two isoforms, GSK-3 (51 kDa) and GSK-3 (47 kDa), which are encoded by separate genes that produce highly ho

  • Glycogen Synthase Kinase 3α specific regulation of murine hepatic Glycogen metabolism
    Cell Metabolism, 2007
    Co-Authors: Katrina Macaulay, Satish Patel, Bradley W Doble, Elaine M Sinclair, Daniel J Drucker, Tanya Hansotia, Andras Nagy, James R Woodgett
    Abstract:

    SUMMARY Glycogen Synthase Kinase 3 comprises two isoforms (GSK-3a and GSK-3b) that are implicated in type II diabetes, neurodegeneration, and cancer. GSK-3 activity is elevated in human and rodent models of diabetes, and various GSK-3 inhibitors improve glucose tolerance and insulin sensitivity in rodent models of obesity and diabetes. Here, we report the generation of mice lacking GSK-3a. Unlike GSK-3b mutants, which die before birth, GSK-3aknockout (GSK-3a KO) animals are viable but display enhanced glucose and insulin sensitivity accompanied by reduced fat mass. Fasted and glucose-stimulated hepatic Glycogen content was enhanced in GSK-3a KO mice, whereas muscle Glycogen was unaltered. Insulin-stimulated protein Kinase B (PKB/Akt) and GSK-3b phosphorylation was higher in GSK3a KO livers compared to wild-type littermates, and IRS-1 expression was markedly increased. We conclude that GSK-3 isoforms exhibit tissue-specific physiological functions and that GSK-3a KO mice are insulin sensitive, reinforcing the potential of GSK-3 as a therapeutic target for type II diabetes.

  • phosphorylation and inactivation of Glycogen Synthase Kinase 3 by protein Kinase a
    Proceedings of the National Academy of Sciences of the United States of America, 2000
    Co-Authors: Xianjun Fang, James R Woodgett, Shuang Xing Yu, Yiling Lu, Robert C Bast, Gordon B Mills
    Abstract:

    Glycogen Synthase Kinase 3 (GSK-3) is implicated in multiple biological processes including metabolism, gene expression, cell fate determination, proliferation, and survival. GSK-3 activity is inhibited through phosphorylation of serine 21 in GSK-3α and serine 9 in GSK-3β. These serine residues of GSK-3 have been previously identified as targets of protein Kinase B (PKB/Akt), a serine/threonine Kinase located downstream of phosphatidylinositol 3-Kinase. Here, we show that serine 21 in GSK-3α and serine 9 in GSK-3β are also physiological substrates of cAMP-dependent protein Kinase A. Protein Kinase A physically associates with, phosphorylates, and inactivates both isoforms of GSK-3. The results indicate that depending on the stimulatory context, the activity of GSK-3 can be modulated either by growth factors that work through the phosphatidylinositol 3-Kinase–protein Kinase B cascade or by hormonal stimulation of G protein-coupled receptors that link to changes in intracellular cAMP levels.

  • Glycogen Synthase Kinase 3β is a negative regulator of cardiomyocyte hypertrophy
    Journal of Cell Biology, 2000
    Co-Authors: Gabriel Choukroun, James R Woodgett, Zhao Bin Kang, Hardeep Ranu, Takashi Matsui, Anthony Rosenzweig, Jeffrey D Molkentin, Alessandro Alessandrini, Roger J Hajjar, Ashour Michael
    Abstract:

    Hypertrophy is a basic cellular response to a variety of stressors and growth factors, and has been best characterized in myocytes. Pathologic hypertrophy of cardiac myocytes leads to heart failure, a major cause of death and disability in the developed world. Several cytosolic signaling pathways have been identified that transduce prohypertrophic signals, but to date, little work has focused on signaling pathways that might negatively regulate hypertrophy. Herein, we report that Glycogen Synthase Kinase-3β (GSK-3β), a protein Kinase previously implicated in processes as diverse as development and tumorigenesis, is inactivated by hypertrophic stimuli via a phosphoinositide 3-Kinase–dependent protein Kinase that phosphorylates GSK-3β on ser 9. Using adenovirus-mediated gene transfer of GSK-3β containing a ser 9 to alanine mutation, which prevents inactivation by hypertrophic stimuli, we demonstrate that inactivation of GSK-3β is required for cardiomyocytes to undergo hypertrophy. Furthermore, our data suggest that GSK-3β regulates the hypertrophic response, at least in part, by modulating the nuclear/cytoplasmic partitioning of a member of the nuclear factor of activated T cells family of transcription factors. The identification of GSK-3β as a transducer of antihypertrophic signals suggests that novel therapeutic strategies to treat hypertrophic diseases of the heart could be designed that target components of the GSK-3 pathway.

Eleonore Beurel - One of the best experts on this subject based on the ideXlab platform.

  • Glycogen Synthase Kinase 3 gsk3 regulation actions and diseases
    Pharmacology & Therapeutics, 2015
    Co-Authors: Eleonore Beurel, Steven F Grieco, Richard S Jope
    Abstract:

    Glycogen Synthase Kinase-3 (GSK3) may be the busiest Kinase in most cells, with over 100 known substrates to deal with. How does GSK3 maintain control to selectively phosphorylate each substrate, and why was it evolutionarily favorable for GSK3 to assume such a large responsibility? GSK3 must be particularly adaptable for incorporating new substrates into its repertoire, and we discuss the distinct properties of GSK3 that may contribute to its capacity to fulfill its roles in multiple signaling pathways. The mechanisms regulating GSK3 (predominantly post-translational modifications, substrate priming, cellular trafficking, protein complexes) have been reviewed previously, so here we focus on newly identified complexities in these mechanisms, how each of these regulatory mechanism contributes to the ability of GSK3 to select which substrates to phosphorylate, and how these mechanisms may have contributed to its adaptability as new substrates evolved. The current understanding of the mechanisms regulating GSK3 is reviewed, as are emerging topics in the actions of GSK3, particularly its interactions with receptors and receptor-coupled signal transduction events, and differential actions and regulation of the two GSK3 isoforms, GSK3α and GSK3β. Another remarkable characteristic of GSK3 is its involvement in many prevalent disorders, including psychiatric and neurological diseases, inflammatory diseases, cancer, and others. We address the feasibility of targeting GSK3 therapeutically, and provide an update of its involvement in the etiology and treatment of several disorders.

  • Glycogen Synthase Kinase 3 inhibitors rescuers of cognitive impairments
    Pharmacology & Therapeutics, 2014
    Co-Authors: Margaret K King, Richard S Jope, Marta Pardo, Yuyan Cheng, Kimberlee Downey, Eleonore Beurel
    Abstract:

    Impairment of cognitive processes is a devastating outcome of many diseases, injuries, and drugs affecting the central nervous system (CNS). Most often, very little can be done by available therapeutic interventions to improve cognitive functions. Here we review evidence that inhibition of Glycogen Synthase Kinase-3 (GSK3) ameliorates cognitive deficits in a wide variety of animal models of CNS diseases, including Alzheimer's disease, Fragile X syndrome, Down syndrome, Parkinson's disease, spinocerebellar ataxia type 1, traumatic brain injury, and others. GSK3 inhibitors also improve cognition following impairments caused by therapeutic interventions, such as cranial irradiation for brain tumors. These findings demonstrate that GSK3 inhibitors are able to ameliorate cognitive impairments caused by a diverse array of diseases, injury, and treatments. The improvements in impaired cognition instilled by administration of GSK3 inhibitors appear to involve a variety of different mechanisms, such as supporting long-term potentiation and diminishing long-term depression, promotion of neurogenesis, reduction of inflammation, and increasing a number of neuroprotective mechanisms. The potential for GSK3 inhibitors to repair cognitive deficits associated with many conditions warrants further investigation of their potential for therapeutic interventions, particularly considering the current dearth of treatments available to reduce loss of cognitive functions.

  • inhibition of Glycogen Synthase Kinase 3 is necessary for the rapid antidepressant effect of ketamine in mice
    Molecular Psychiatry, 2011
    Co-Authors: Eleonore Beurel, Ling Song, Richard S Jope
    Abstract:

    Inhibition of Glycogen Synthase Kinase-3 is necessary for the rapid antidepressant effect of ketamine in mice

  • innate and adaptive immune responses regulated by Glycogen Synthase Kinase 3 gsk3
    Trends in Immunology, 2010
    Co-Authors: Eleonore Beurel, Suzanne M Michalek, Richard S Jope
    Abstract:

    In just a few years, the view of Glycogen Synthase Kinase-3 (GSK3) has been transformed from an obscure enzyme seldom encountered in the immune literature to one implicated in an improbably large number of roles. GSK3 is a crucial regulator of the balance between pro- and anti-inflammatory cytokine production in both the periphery and the central nervous system, so that GSK3 inhibitors such as lithium can diminish inflammation. GSK3 influences T-cell proliferation, differentiation and survival. Many effects stem from GSK3 regulation of critical transcription factors, such as NF-κB, NFAT and STATs. These discoveries led to the rapid application of GSK3 inhibitors to animal models of sepsis, arthritis, colitis, multiple sclerosis and others, demonstrating their potential for therapeutic intervention.

  • Glycogen Synthase Kinase 3 gsk3 inflammation diseases and therapeutics
    Neurochemical Research, 2007
    Co-Authors: Richard S Jope, Christopher J Yuskaitis, Eleonore Beurel
    Abstract:

    Deciphering what governs inflammation and its effects on tissues is vital for understanding many pathologies. The recent discovery that Glycogen Synthase Kinase-3 (GSK3) promotes inflammation reveals a new component of its well-documented actions in several prevalent diseases which involve inflammation, including mood disorders, Alzheimer’s disease, diabetes, and cancer. Involvement in such disparate conditions stems from the widespread influences of GSK3 on many cellular functions, with this review focusing on its regulation of inflammatory processes. GSK3 promotes the production of inflammatory molecules and cell migration, which together make GSK3 a powerful regulator of inflammation, while GSK3 inhibition provides protection from inflammatory conditions in animal models. The involvement of GSK3 and inflammation in these diseases are highlighted. Thus, GSK3 may contribute not only to primary pathologies in these diseases, but also to the associated inflammation, suggesting that GSK3 inhibitors may have multiple effects influencing these conditions.

Benjamin C. Naman - One of the best experts on this subject based on the ideXlab platform.

  • eckmaxol a phlorotannin extracted from ecklonia maxima produces anti β amyloid oligomer neuroprotective effects possibly via directly acting on Glycogen Synthase Kinase 3β
    ACS Chemical Neuroscience, 2018
    Co-Authors: Jialing Wang, Jiachen Zheng, Chunhui Huang, Jiaying Zhao, Jiajia Lin, Xuezhen Zhou, Benjamin C. Naman, Ning Wang, William H. Gerwick
    Abstract:

    Alzheimer’s disease is a progressive neurodegenerative disorder that mainly affects the elderly. Soluble β-amyloid oligomer, which can induce neurotoxicity, is generally regarded as the main neurotoxin in Alzheimer’s disease. Here we report that eckmaxol, a phlorotannin extracted from the brown alga Ecklonia maxima, could produce neuroprotective effects in SH-SY5Y cells. Eckmaxol effectively prevented but did not rescue β-amyloid oligomer-induced neuronal apoptosis and increase of intracellular reactive oxygen species. Eckmaxol also significantly reversed the decreased expression of phospho-Ser9-Glycogen Synthase Kinase 3β and increased expression of phospho-extracellular signal-regulated Kinase, which was induced by Aβ oligomer. Moreover, both Glycogen Synthase Kinase 3β and mitogen activated protein Kinase inhibitors produced neuroprotective effects in SH-SY5Y cells. Furthermore, eckmaxol showed favorable interaction in the ATP binding site of Glycogen Synthase Kinase 3β and mitogen activated protein ki...

  • Eckmaxol, a Phlorotannin Extracted from Ecklonia maxima, Produces Anti-β-amyloid Oligomer Neuroprotective Effects Possibly via Directly Acting on Glycogen Synthase Kinase 3β
    2018
    Co-Authors: Jialing Wang, Jiachen Zheng, Chunhui Huang, Jiaying Zhao, Jiajia Lin, Xuezhen Zhou, Benjamin C. Naman, Ning Wang, William H. Gerwick, Qinwen Wang
    Abstract:

    Alzheimer’s disease is a progressive neurodegenerative disorder that mainly affects the elderly. Soluble β-amyloid oligomer, which can induce neurotoxicity, is generally regarded as the main neurotoxin in Alzheimer’s disease. Here we report that eckmaxol, a phlorotannin extracted from the brown alga Ecklonia maxima, could produce neuroprotective effects in SH-SY5Y cells. Eckmaxol effectively prevented but did not rescue β-amyloid oligomer-induced neuronal apoptosis and increase of intracellular reactive oxygen species. Eckmaxol also significantly reversed the decreased expression of phospho-Ser9-Glycogen Synthase Kinase 3β and increased expression of phospho-extracellular signal-regulated Kinase, which was induced by Aβ oligomer. Moreover, both Glycogen Synthase Kinase 3β and mitogen activated protein Kinase inhibitors produced neuroprotective effects in SH-SY5Y cells. Furthermore, eckmaxol showed favorable interaction in the ATP binding site of Glycogen Synthase Kinase 3β and mitogen activated protein Kinase. These results suggested that eckmaxol might produce neuroprotective effects via concurrent inhibition of Glycogen Synthase Kinase 3β and extracellular signal-regulated Kinase pathways, possibly via directly acting on Glycogen Synthase Kinase 3β and mitogen activated protein Kinase. Based on the central role that β-amyloid oligomers play in the pathogenesis of Alzheimer’s disease and the high annual production of Ecklonia maxima for alginate and other nutritional ingredients, this report represents a new candidate for the treatment of Alzheimer’s disease, and also expands the potential application of Ecklonia maxima and its constituents in the field of pharmacology