De Maw Chuang

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. ncbi request reprint PET imaging with [11C]PBR28 can localize and quantify upregulated peripheral benzodiazepine receptors associated with cerebral ischemia in rat
    Masao Imaizumi
    Molecular Imaging Branch, National Institute of Mental Health, National Institutes of Health, Building 1, Room B3 10, 1 Center Drive, MSC 0135, Bethesda, MD 20892 0135, USA
    Neurosci Lett 411:200-5. 2007
  2. pmc GSK-3 as a Target for Lithium-Induced Neuroprotection Against Excitotoxicity in Neuronal Cultures and Animal Models of Ischemic Stroke
    De Maw Chuang
    Molecular Neurobiology Section, National Institute of Mental Health, National Institutes of Health Bethesda, MD, USA
    Front Mol Neurosci 4:15. 2011
  3. pmc Multiple roles of HDAC inhibition in neurodegenerative conditions
    De Maw Chuang
    Molecular Neurobiology Section, National Institute of Mental Health, National Institutes of Health, 10 Center Drive MSC 1363, Bethesda, MD 20892 1363, USA
    Trends Neurosci 32:591-601. 2009
  4. ncbi request reprint Glyceraldehyde-3-phosphate dehydrogenase, apoptosis, and neurodegenerative diseases
    De Maw Chuang
    Molecular Neurobiology Section, Mood and Anxiety Disorders Program, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892 1363, USA
    Annu Rev Pharmacol Toxicol 45:269-90. 2005
  5. ncbi request reprint Short-term lithium treatment promotes neuronal survival and proliferation in rat striatum infused with quinolinic acid, an excitotoxic model of Huntington's disease
    V V Senatorov
    Molecular Neurobiology Section, National Institute of Mental Health, National Institutes of Health, Bethesda, MD, USA
    Mol Psychiatry 9:371-85. 2004
  6. pmc In search of the Holy Grail for the treatment of neurodegenerative disorders: has a simple cation been overlooked?
    De Maw Chuang
    Mood and Anxiety Disorders Program, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892 1363, USA
    Biol Psychiatry 62:4-6. 2007
  7. ncbi request reprint The antiapoptotic actions of mood stabilizers: molecular mechanisms and therapeutic potentials
    De Maw Chuang
    Molecular Neurobiology Section, Biological Psychiatry Branch, Mood and Anxiety Disorders Program, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892 1363, USA
    Ann N Y Acad Sci 1053:195-204. 2005
  8. ncbi request reprint Neuroprotective and neurotrophic actions of the mood stabilizer lithium: can it be used to treat neurodegenerative diseases?
    De Maw Chuang
    Molecular Neurobiology Section, Mood and Anxiety Disorders Program, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892 1363, USA
    Crit Rev Neurobiol 16:83-90. 2004
  9. ncbi request reprint Endogenous alpha-synuclein is induced by valproic acid through histone deacetylase inhibition and participates in neuroprotection against glutamate-induced excitotoxicity
    Yan Leng
    Molecular Neurobiology Section, Biological Psychiatry Branch, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892 1363, USA
    J Neurosci 26:7502-12. 2006
  10. ncbi request reprint Regulation of c-Jun N-terminal kinase, p38 kinase and AP-1 DNA binding in cultured brain neurons: roles in glutamate excitotoxicity and lithium neuroprotection
    Ren Wu Chen
    Molecular Neurobiology Section, Mood and Anxiety Disorders Program, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland, USA
    J Neurochem 84:566-75. 2003

Collaborators

Detail Information

Publications62

  1. ncbi request reprint PET imaging with [11C]PBR28 can localize and quantify upregulated peripheral benzodiazepine receptors associated with cerebral ischemia in rat
    Masao Imaizumi
    Molecular Imaging Branch, National Institute of Mental Health, National Institutes of Health, Building 1, Room B3 10, 1 Center Drive, MSC 0135, Bethesda, MD 20892 0135, USA
    Neurosci Lett 411:200-5. 2007
    ..In this first study to demonstrate neuroinflammation in vivo with small animal PET, [11C]PBR28 had adequate sensitivity to localize and quantify the associated increase in PBRs...
  2. pmc GSK-3 as a Target for Lithium-Induced Neuroprotection Against Excitotoxicity in Neuronal Cultures and Animal Models of Ischemic Stroke
    De Maw Chuang
    Molecular Neurobiology Section, National Institute of Mental Health, National Institutes of Health Bethesda, MD, USA
    Front Mol Neurosci 4:15. 2011
    ..Several other GSK-3 inhibitors have also been reported to be beneficial in rodent ischemic models. Together, GSK-3 inhibition is a rational strategy to combat ischemic stroke and other excitotoxicity-related brain disorders...
  3. pmc Multiple roles of HDAC inhibition in neurodegenerative conditions
    De Maw Chuang
    Molecular Neurobiology Section, National Institute of Mental Health, National Institutes of Health, 10 Center Drive MSC 1363, Bethesda, MD 20892 1363, USA
    Trends Neurosci 32:591-601. 2009
    ..We discuss the targets and mechanisms underlying these effects of HDAC inhibition and comment on the potential for some HDAC inhibitors to prove clinically effective in the treatment of neurodegenerative disorders...
  4. ncbi request reprint Glyceraldehyde-3-phosphate dehydrogenase, apoptosis, and neurodegenerative diseases
    De Maw Chuang
    Molecular Neurobiology Section, Mood and Anxiety Disorders Program, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892 1363, USA
    Annu Rev Pharmacol Toxicol 45:269-90. 2005
    ..The interaction of GAPDH with disease-related proteins as well as drugs used to treat these diseases suggests that it is a potential molecular target for drug development...
  5. ncbi request reprint Short-term lithium treatment promotes neuronal survival and proliferation in rat striatum infused with quinolinic acid, an excitotoxic model of Huntington's disease
    V V Senatorov
    Molecular Neurobiology Section, National Institute of Mental Health, National Institutes of Health, Bethesda, MD, USA
    Mol Psychiatry 9:371-85. 2004
    ....
  6. pmc In search of the Holy Grail for the treatment of neurodegenerative disorders: has a simple cation been overlooked?
    De Maw Chuang
    Mood and Anxiety Disorders Program, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892 1363, USA
    Biol Psychiatry 62:4-6. 2007
  7. ncbi request reprint The antiapoptotic actions of mood stabilizers: molecular mechanisms and therapeutic potentials
    De Maw Chuang
    Molecular Neurobiology Section, Biological Psychiatry Branch, Mood and Anxiety Disorders Program, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892 1363, USA
    Ann N Y Acad Sci 1053:195-204. 2005
    ..Thus, lithium and valproate are potential drugs for treating some forms of neurodegenerative diseases...
  8. ncbi request reprint Neuroprotective and neurotrophic actions of the mood stabilizer lithium: can it be used to treat neurodegenerative diseases?
    De Maw Chuang
    Molecular Neurobiology Section, Mood and Anxiety Disorders Program, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892 1363, USA
    Crit Rev Neurobiol 16:83-90. 2004
    ..In addition to its present use in bipolar patients, lithium could be used to treat acute brain injuries such as stroke and chronic progressive neurodegenerative diseases...
  9. ncbi request reprint Endogenous alpha-synuclein is induced by valproic acid through histone deacetylase inhibition and participates in neuroprotection against glutamate-induced excitotoxicity
    Yan Leng
    Molecular Neurobiology Section, Biological Psychiatry Branch, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892 1363, USA
    J Neurosci 26:7502-12. 2006
    ..Clinically, VPA may represent a suitable treatment for excitotoxicity-related neurodegenerative diseases...
  10. ncbi request reprint Regulation of c-Jun N-terminal kinase, p38 kinase and AP-1 DNA binding in cultured brain neurons: roles in glutamate excitotoxicity and lithium neuroprotection
    Ren Wu Chen
    Molecular Neurobiology Section, Mood and Anxiety Disorders Program, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland, USA
    J Neurochem 84:566-75. 2003
    ..Moreover, the neuroprotective effects of lithium are mediated, at least in part, by suppressing NMDA receptor-mediated activation of the mitogen-activated protein kinase pathway...
  11. ncbi request reprint Histone deacetylase inhibitors exhibit anti-inflammatory and neuroprotective effects in a rat permanent ischemic model of stroke: multiple mechanisms of action
    Hyeon Ju Kim
    Molecular Neurobiology Section, National Institute of Mental Health, National Institutes of Health, Building 10, Bethesda, MD 20892 1363, USA
    J Pharmacol Exp Ther 321:892-901. 2007
    ..Given that there is no effective treatment for stroke, HDAC inhibitors, such as VPA, SB, and TSA, should be evaluated for their potential use for clinical trials in stroke patients...
  12. ncbi request reprint Valproic acid reduces brain damage induced by transient focal cerebral ischemia in rats: potential roles of histone deacetylase inhibition and heat shock protein induction
    Ming Ren
    Molecular Neurobiology Section, National Institute of Mental Health, National Institutes of Health, 10 Center Drive, MSC 1363, Bethesda, MD 20892 1363, USA
    J Neurochem 89:1358-67. 2004
    ..Altogether, our results demonstrate that VPA is neuroprotective in the cerebral ischemia model and suggest that the protection mechanisms may involve HDAC inhibition and HSP induction...
  13. doi request reprint Synergistic neuroprotective effects of lithium and valproic acid or other histone deacetylase inhibitors in neurons: roles of glycogen synthase kinase-3 inhibition
    Yan Leng
    Molecular Neurobiology Section, Mood and Anxiety Disorders Program, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892 1363, USA
    J Neurosci 28:2576-88. 2008
    ..Our results may have implications for the combined use of lithium and VPA in treating bipolar disorder. Additionally, combined use of both drugs may be warranted for clinical trials to treat glutamate-related neurodegenerative diseases...
  14. pmc Valproic acid induces functional heat-shock protein 70 via Class I histone deacetylase inhibition in cortical neurons: a potential role of Sp1 acetylation
    Zoya Marinova
    Molecular Neurobiology Section, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892 1363, USA
    J Neurochem 111:976-87. 2009
    ....
  15. ncbi request reprint Lithium protection against glutamate excitotoxicity in rat cerebral cortical neurons: involvement of NMDA receptor inhibition possibly by decreasing NR2B tyrosine phosphorylation
    Ryota Hashimoto
    Section on Molecular Neurobiology, Mood and Anxiety Disorder Program, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892 1363, USA
    J Neurochem 80:589-97. 2002
    ..This action could also be relevant to its clinical efficacy for bipolar patients...
  16. pmc Chronic valproate treatment enhances postischemic angiogenesis and promotes functional recovery in a rat model of ischemic stroke
    Zhifei Wang
    Molecular Neurobiology Section, NIMH, NIH, 10 Center Drive, MSC 1363, Bethesda, MD 20892 1363, USA
    Stroke 43:2430-6. 2012
    ..The present study investigated whether VPA could enhance angiogenesis and promote long-term functional recovery after ischemic stroke...
  17. ncbi request reprint Neuroprotective effects of lithium in cultured cells and animal models of diseases
    De Maw Chuang
    Section on Molecular Neurobiology, Mood and Anxiety Disorder Program, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892 1363, USA
    Bipolar Disord 4:129-36. 2002
    ..Our results suggest that lithium might have utility in the treatment of neurodegenerative disorders in addition to its common use for the treatment of bipolar depressive patients...
  18. ncbi request reprint Potential roles of HDAC inhibitors in mitigating ischemia-induced brain damage and facilitating endogenous regeneration and recovery
    Emily B Fessler
    Molecular Neurobiology Section, National Institute of Mental Health, National Institutes of Health, 10 Center Dr, MSC 1363, Bethesda, MD 20892 1363, USA
    Curr Pharm Des 19:5105-20. 2013
    ..In the following review, we discuss the mechanisms by which HDAC inhibitors exert these protective effects and provide evidence for their strong potential to ultimately improve stroke outcome in patients. ..
  19. doi request reprint Neuroprotective effects of the mood stabilizer lamotrigine against glutamate excitotoxicity: roles of chromatin remodelling and Bcl-2 induction
    Yan Leng
    Molecular Neurobiology Section, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892 1363, USA
    Int J Neuropsychopharmacol 16:607-20. 2013
    ..These underlying mechanisms may contribute to the clinical efficacy of LTG in treating bipolar disorder and warrant further investigation...
  20. doi request reprint Posttrauma cotreatment with lithium and valproate: reduction of lesion volume, attenuation of blood-brain barrier disruption, and improvement in motor coordination in mice with traumatic brain injury
    Fengshan Yu
    Section on Molecular Neurobiology, National Institute of Mental Health, National Institutes of Health, 10 Center Dr, MSC 1363, Bethesda, MD 20892, USA
    J Neurosurg 119:766-73. 2013
    ....
  21. pmc Histone deacetylase inhibition alters histone methylation associated with heat shock protein 70 promoter modifications in astrocytes and neurons
    Zoya Marinova
    Molecular Neurobiology Section, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892 1363, USA
    Neuropharmacology 60:1109-15. 2011
    ..This article is part of a Special Issue entitled 'Trends in neuropharmacology: in memory of Erminio Costa'...
  22. ncbi request reprint Lithium induces brain-derived neurotrophic factor and activates TrkB in rodent cortical neurons: an essential step for neuroprotection against glutamate excitotoxicity
    Ryota Hashimoto
    Molecular Neurobiology Section, Mood and Anxiety Disorders Program, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892 1363, USA
    Neuropharmacology 43:1173-9. 2002
    ..Taken together, these data suggest that the BDNF/TrkB pathway plays an essential role in mediating the neuroprotective effect of lithium...
  23. pmc Therapeutic potential of mood stabilizers lithium and valproic acid: beyond bipolar disorder
    Chi Tso Chiu
    Molecular Neurobiology Section, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland, USA
    Pharmacol Rev 65:105-42. 2013
    ....
  24. ncbi request reprint Lithium-induced inhibition of Src tyrosine kinase in rat cerebral cortical neurons: a role in neuroprotection against N-methyl-D-aspartate receptor-mediated excitotoxicity
    Ryota Hashimoto
    Mood and Anxiety Disorders Program, National Institute of Mental Health, National Institutes of Health, Bldg 10, Rm 4C 206, 10 Center Dr MSC 1363, Bethesda, MD 20892 1363, USA
    FEBS Lett 538:145-8. 2003
    ..Our results suggest that lithium-induced inactivation of Src kinase contributes to this drug-induced NMDA receptor inhibition and neuroprotection against excitotoxicity...
  25. pmc Lithium reduces BACE1 overexpression, β amyloid accumulation, and spatial learning deficits in mice with traumatic brain injury
    Fengshan Yu
    Section on Molecular Neurobiology, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Neurotrauma 29:2342-51. 2012
    ..Our findings suggest that lithium is a potentially useful agent for managing memory impairments after TBI or other head trauma...
  26. pmc Mesenchymal stem cells primed with valproate and lithium robustly migrate to infarcted regions and facilitate recovery in a stroke model
    Li Kai Tsai
    Molecular Neurobiology Section, National Institute of Mental Health, National Institutes of Health, 10 Center Dr, MSC 1363, Bethesda, MD 20892 1363, USA
    Stroke 42:2932-9. 2011
    ..Ability of VPA and lithium to promote MSC homing and to improve functional recovery was assessed in a rat model of cerebral ischemia...
  27. pmc Valproic acid attenuates blood-brain barrier disruption in a rat model of transient focal cerebral ischemia: the roles of HDAC and MMP-9 inhibition
    Zhifei Wang
    Molecular Neurobiology Section, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892 1363, USA
    J Cereb Blood Flow Metab 31:52-7. 2011
    ..Sodium butyrate, another HDAC inhibitor, mimicked these effects of VPA. Our findings suggest that BBB protection by VPA involves HDAC inhibition-mediated suppression of NF-κB activation, MMP-9 induction, and tight junction degradation...
  28. pmc The mood stabilizers valproic acid and lithium enhance mesenchymal stem cell migration via distinct mechanisms
    Li Kai Tsai
    Section on Molecular Neurobiology, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892 1363, USA
    Neuropsychopharmacology 35:2225-37. 2010
    ..Combining VPA and lithium treatment further increased MSC migration. Overall, VPA and lithium stimulated MSC migration through distinct targets and mediators: HDAC-CXCR4 and GSK-3β-MMP-9, respectively...
  29. ncbi request reprint Lithium neuroprotection: molecular mechanisms and clinical implications
    Michael K Rowe
    Molecular Neurobiology Section, National Institute of Mental Health, National Institutes of Health Building 10, Room 4C206, 10 Center Drive, MSC 1363, Bethesda, MD 20892 1363, USA
    Expert Rev Mol Med 6:1-18. 2004
    ....
  30. pmc Potent neuroprotective effects of novel structural derivatives of valproic acid: potential roles of HDAC inhibition and HSP70 induction
    Yan Leng
    Molecular Neurobiology Section, National Institute of Mental Health, National Institutes of Health, Bldg 10, Rm 3D 38, 10 Center Dr, Bethesda, MD 20892 1363, USA
    Neurosci Lett 476:127-32. 2010
    ..Our results suggest that these two VPA derivatives may ultimately be developed into potent neuroprotective drugs in preclinical and clinical studies...
  31. ncbi request reprint Regulation and function of glycogen synthase kinase-3 isoforms in neuronal survival
    Min Huei Liang
    Molecular Neurobiology Section, National Institute of Mental Health, Bethesda, Maryland 20892 1363, USA
    J Biol Chem 282:3904-17. 2007
    ..The development of GSK-3 isoform-specific inhibitors seems to be warranted for treating GSK-3-mediated pathology...
  32. ncbi request reprint Differential roles of glycogen synthase kinase-3 isoforms in the regulation of transcriptional activation
    Min Huei Liang
    Molecular Neurobiology Section, National Institute of Mental Health, Bethesda, Maryland 20892 1363, USA
    J Biol Chem 281:30479-84. 2006
    ..The development of GSK-3 isoform-specific inhibitors is thus crucial for therapeutic intervention of GSK-3-related neuropathological conditions...
  33. ncbi request reprint Valproic acid, a mood stabilizer and anticonvulsant, protects rat cerebral cortical neurons from spontaneous cell death: a role of histone deacetylase inhibition
    Mi Ra Jeong
    Molecular Neurobiology Section, National Institute of Mental Health, National Institutes of Health, Bldg 10, Rm 4C 206, 10 Center Dr MSC 1363, Bethesda, MD 20892 1363, USA
    FEBS Lett 542:74-8. 2003
    ..Our results suggest a role of histone deacetylase inhibition in mediating the neuroprotective action of VPA...
  34. pmc Lithium inhibits Smad3/4 transactivation via increased CREB activity induced by enhanced PKA and AKT signaling
    Min Huei Liang
    Molecular Neurobiology Section, National Institute of Mental Health, National Institutes of Health, 10 Center Dr MSC 1363, Bethesda, MD, USA
    Mol Cell Neurosci 37:440-53. 2008
    ..Therapeutic implications of our findings are discussed...
  35. pmc Postinsult treatment with lithium reduces brain damage and facilitates neurological recovery in a rat ischemia/reperfusion model
    Ming Ren
    Molecular Neurobiology Section, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892 1363, USA
    Proc Natl Acad Sci U S A 100:6210-5. 2003
    ..Moreover, the heat shock response is likely to be involved in lithium's neuroprotective actions. Additionally, our studies indicate that lithium may have clinical utility for the treatment of patients with acute stroke...
  36. pmc Lentivirally mediated GSK-3β silencing in the hippocampal dentate gyrus induces antidepressant-like effects in stressed mice
    Naoto Omata
    Molecular Neurobiology Section, National Institute of Mental Health, National Institutes of Health, Bethesda, MD, USA
    Int J Neuropsychopharmacol 14:711-7. 2011
    ..To our knowledge, this is the first demonstration that a single injection of lentivirus-expressing GSK-3β shRNA in the hippocampal dentate gyrus of chronically stressed mice has antidepressant-like effects elicited by gene silencing...
  37. pmc Lithium ameliorates neurodegeneration, suppresses neuroinflammation, and improves behavioral performance in a mouse model of traumatic brain injury
    Fengshan Yu
    Section on Molecular Neurobiology, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland, USA
    J Neurotrauma 29:362-74. 2012
    ..Our results support the notion that lithium has heretofore unrecognized capacity to mitigate the neurodegenerative effects and improve functional outcomes in TBI...
  38. pmc Neuroprotective action of lithium in disorders of the central nervous system
    Chi Tso Chiu
    Section on Molecular Neurobiology, National Institute of Mental Health, National Institutes of Health, 10 Center Drive MSC 1363, Bethesda, MD 20892 1363, USA
    Zhong Nan Da Xue Xue Bao Yi Xue Ban 36:461-76. 2011
    ....
  39. pmc Combined treatment with the mood stabilizers lithium and valproate produces multiple beneficial effects in transgenic mouse models of Huntington's disease
    Chi Tso Chiu
    Section on Molecular Neurobiology, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892 1363, USA
    Neuropsychopharmacology 36:2406-21. 2011
    ....
  40. pmc Histone deacetylase inhibitors up-regulate astrocyte GDNF and BDNF gene transcription and protect dopaminergic neurons
    Xuefei Wu
    Laboratory of Pharmacology and Chemistry, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC, USA
    Int J Neuropsychopharmacol 11:1123-34. 2008
    ..This study indicates that astrocytes may be a critical neuroprotective mechanism of HDAC inhibitors, revealing a novel target for the treatment of psychiatric and neurodegenerative diseases...
  41. ncbi request reprint Overexpression and nuclear accumulation of glyceraldehyde-3-phosphate dehydrogenase in a transgenic mouse model of Huntington's disease
    Vladimir V Senatorov
    Molecular Neurobiology Section, Mood and Anxiety Disorders Program, National Institute of Mental Health, National Institutes of Health, MD 20892 1363, Bethesda, USA
    Mol Cell Neurosci 22:285-97. 2003
    ..Thus, we conclude that mutation of huntingtin is associated with GAPDH overexpression and nuclear translocation in discrete populations of brain neurons...
  42. pmc GSK-3 is a viable potential target for therapeutic intervention in bipolar disorder
    Michael K Rowe
    Molecular Neurobiology Section, Mood and Anxiety Disorders Program, National Institute of Mental Health, National Institutes of Health, Building 10, Room 4C206, 10 Center Drive, MSC 1363, Bethesda, MD 20892 1363, USA
    Neurosci Biobehav Rev 31:920-31. 2007
    ..Taken together, the evidence suggests that targeting GSK-3 may be a means to control the symptoms of bipolar disorder...
  43. pmc The HDAC inhibitor, sodium butyrate, stimulates neurogenesis in the ischemic brain
    Hyeon Ju Kim
    Molecular Neurobiology Section, Mood and Anxiety Disorders Program, National Institute of Mental Health, Bethesda, MD 20892 1363, USA
    J Neurochem 110:1226-40. 2009
    ....
  44. pmc Molecular actions and therapeutic potential of lithium in preclinical and clinical studies of CNS disorders
    Chi Tso Chiu
    Molecular Neurobiology Section, Mood and Anxiety Disorders Program, National Institute of Mental Health, National Institutes of Health, 10 Center Drive MSC 1363, Bethesda, MD 20892 1363, USA
    Pharmacol Ther 128:281-304. 2010
    ..This article reviews the most recent findings regarding the potential targets involved in lithium's neuroprotective effects, and the implication of these findings for the treatment of a variety of diseases...
  45. doi request reprint Beneficial effects of mood stabilizers lithium, valproate and lamotrigine in experimental stroke models
    Zhi Fei Wang
    Molecular Neurobiology Section, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892 1363, USA
    Acta Pharmacol Sin 32:1433-45. 2011
    ..We also propose several future research avenues that may extend our understanding of the benefits of lithium, valproate and lamotrigine in improving stroke outcomes...
  46. pmc Bax inhibitor 1, a modulator of calcium homeostasis, confers affective resilience
    Joshua G Hunsberger
    National Institute of Mental Health, National Institutes of Health, Bethesda, MD, USA
    Brain Res 1403:19-27. 2011
    ..Together, these data suggest that BI-1, through its actions on calcium homeostasis, may confer affective resiliency in multiple animal models of depression and anhedonia...
  47. ncbi request reprint Protracted lithium treatment protects against the ER stress elicited by thapsigargin in rat PC12 cells: roles of intracellular calcium, GRP78 and Bcl-2
    T Hiroi
    Molecular Neurobiology Section, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892 1363, USA
    Pharmacogenomics J 5:102-11. 2005
    ..Additionally, thapsigargin-induced cytotoxicity was suppressed by pretreatment with another mood-stabilizer, valproate, indicating that cytoprotection against ER stress is a common action of mood-stabilizing drugs...
  48. pmc Mood stabilizer-regulated miRNAs in neuropsychiatric and neurodegenerative diseases: identifying associations and functions
    Joshua G Hunsberger
    Molecular Neurobiology Section, National Institute of Mental Health NIMH, National Institutes of Health Bethesda, MD, USA
    Am J Transl Res 5:450-64. 2013
    ..We anticipate that these associations and overlaps implicate critical pathways and miRNAs in disease mechanisms for novel therapeutic treatments that may hold potential for many neurological diseases...
  49. pmc Lithium ameliorates phenotypic deficits in a mouse model of fragile X syndrome
    Zhong Hua Liu
    Section on Neuroadaptation and Protein Metabolism, National Institute of Mental Health, Bethesda, MD, USA
    Int J Neuropsychopharmacol 14:618-30. 2011
    ..Our findings and those from other laboratories on the efficacy of lithium treatment in animal models support further studies in patients with FXS...
  50. ncbi request reprint Lithium stimulates progenitor proliferation in cultured brain neurons
    R Hashimoto
    Molecular Neurobiology Section, Mood and Anxiety Disorders Program, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892 1363, USA
    Neuroscience 117:55-61. 2003
    ..Cultured brain neurons may provide a valuable model for studying the molecular mechanisms underlying lithium-induced up-regulation of neural proliferation...
  51. pmc Angiotensin II AT1 receptor blockade ameliorates brain inflammation
    Julius Benicky
    Section on Pharmacology, Division of Intramural Research Programs, Department of Health and Human Services, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892, USA
    Neuropsychopharmacology 36:857-70. 2011
    ..Our results indicate that these compounds may offer a novel and safe therapeutic approach for the treatment of brain disorders...
  52. ncbi request reprint Chronic lithium treatment antagonizes glutamate-induced decrease of phosphorylated CREB in neurons via reducing protein phosphatase 1 and increasing MEK activities
    K L Kopnisky
    Molecular Neurobiology Section, National Institute of Mental Health, National Institutes of Health, Building 10 Center Drive, Room 4C206, MSC 1363 Bethesda, MD 20892 1363, USA
    Neuroscience 116:425-35. 2003
    ..Higher levels of phosphorylated CREB and CRE-responsive genes such as bcl-2 may be responsible for lithium's reported effects on neuronal survival...
  53. ncbi request reprint Valproate protects dopaminergic neurons in midbrain neuron/glia cultures by stimulating the release of neurotrophic factors from astrocytes
    P S Chen
    Laboratory of Pharmacology and Chemistry, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC, USA
    Mol Psychiatry 11:1116-25. 2006
    ..Moreover, the neurotrophic effects of VPA may contribute to the therapeutic action of this drug in treating bipolar mood disorder that involves a loss of neurons and glia in discrete brain areas...
  54. ncbi request reprint Neurotrophins protect against cytosine arabinoside-induced apoptosis of immature rat cerebellar neurons
    P Leeds
    Molecular Neurobiology Section, National Institute of Mental Health NIH, 10 Center Drive, MSC 1363, Bethesda, MD 20892 1363, USA
    Neurochem Int 46:61-72. 2005
    ..These results show that neurotrophins protect against AraC-induced apoptosis, at least in part, through TrkB-mediated activation of the PI 3-kinase/Akt and MEK signaling pathways...
  55. ncbi request reprint Valproic acid inhibits histone deacetylase activity and suppresses excitotoxicity-induced GAPDH nuclear accumulation and apoptotic death in neurons
    H Kanai
    Molecular Neurobiology Section, National Institute of Mental Health, National Institutes of Health, Bethesda, MD, USA
    Pharmacogenomics J 4:336-44. 2004
    ....
  56. pmc Valproic acid and other histone deacetylase inhibitors induce microglial apoptosis and attenuate lipopolysaccharide-induced dopaminergic neurotoxicity
    P S Chen
    Laboratory of Pharmacology and Chemistry, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA
    Neuroscience 149:203-12. 2007
    ..Taken together, our results shed light on a novel mechanism whereby HDACIs induce neuroprotection and underscore the potential utility of HDACIs in preventing inflammation-related neurodegenerative disorders such as Parkinson's disease...
  57. pmc Functional MRI of delayed chronic lithium treatment in rat focal cerebral ischemia
    Young R Kim
    Athinoula Martinos Center for Biomedical Imaging Massachusetts General Hospital, 149 13th Street, Room 2301, Charlestown, MA 02129, USA
    Stroke 39:439-47. 2008
    ..We further investigated neurohemodynamic aspects of the treatment-associated recovery by assessing the therapeutic efficacy of delayed chronic lithium treatment using functional MRI...
  58. ncbi request reprint Susceptibility of striatal neurons to excitotoxic injury correlates with basal levels of Bcl-2 and the induction of P53 and c-Myc immunoreactivity
    Zhong qin Liang
    Department of Pharmacology, Soochow University School of Medicine, Suzhou 215007, P R China
    Neurobiol Dis 20:562-73. 2005
    ..The selective vulnerability of striatal medium spiny neurons to degeneration in a rodent model of Huntington's disease appears to correlate with their low levels of Bcl-2-i and high levels of induced p53-i and c-Myc-i...
  59. ncbi request reprint Lithium reduces ischemia-induced hippocampal CA1 damage and behavioral deficits in gerbils
    Qingming Bian
    Department of Anesthesiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, PR China
    Brain Res 1184:270-6. 2007
    ..These results underscore the ability of lithium to improve functional behavioral outcome in gerbil and rodent cerebral ischemic models and further indicate the potential therapeutic use of lithium in certain human stroke conditions...
  60. ncbi request reprint Nuclear factor-kappaB-dependent cyclin D1 induction and DNA replication associated with N-methyl-D-aspartate receptor-mediated apoptosis in rat striatum
    Zhong qin Liang
    Department of Pharmacology, Soochow University School of Medicine, Suzhou, China
    J Neurosci Res 85:1295-309. 2007
    ..Excitotoxin-induced neuronal apoptosis may thus result from, at least partially, a failed cell cycle attempt...
  61. ncbi request reprint [Neuroprotective actions of lithium]
    Ryota Hashimoto
    Seishin Shinkeigaku Zasshi 105:81-6. 2003
    ..Clearly, mood-stabilizers may have expanded use for treating excitotoxin-related neurodegenerative diseases...
  62. ncbi request reprint Valproate pretreatment protects dopaminergic neurons from LPS-induced neurotoxicity in rat primary midbrain cultures: role of microglia
    Giia Sheun Peng
    Department of Neurology, Tri Service General Hospital, National Defense Medical Center, Taipei, Taiwan
    Brain Res Mol Brain Res 134:162-9. 2005
    ..Taken together, our study reinforces the view that VPA may have utility in treating Parkinson's disease...