A M Marini

Summary

Affiliation: Uniformed Services University of the Health Sciences
Country: USA

Publications

  1. ncbi request reprint Preconditioning and neurotrophins: a model for brain adaptation to seizures, ischemia and other stressful stimuli
    A M Marini
    Department of Neurology and Neuroscience Program, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA
    Amino Acids 32:299-304. 2007
  2. ncbi request reprint Toward the development of strategies to prevent ischemic neuronal injury. In vitro studies
    A M Marini
    Department of Neurology, Walter Reed Army Medical Center, Washington, DC, USA
    Ann N Y Acad Sci 825:209-19. 1997
  3. ncbi request reprint Hormesis: a promising strategy to sustain endogenous neuronal survival pathways against neurodegenerative disorders
    Ann M Marini
    Department of Neurology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA
    Ageing Res Rev 7:21-33. 2008
  4. ncbi request reprint Brain adaptation to stressful stimuli: a new perspective on potential therapeutic approaches based on BDNF and NMDA receptors
    Ann M Marini
    Department of Neurology and Neuroscience Program, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814, USA
    CNS Neurol Disord Drug Targets 7:382-90. 2008
  5. ncbi request reprint Transient neurologic deficits associated with carbamazepine-induced hypertension
    Ann M Marini
    Department of Neurology and Neuroscience, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, MD 20814, USA
    Clin Neuropharmacol 26:174-6. 2003
  6. ncbi request reprint Metabolic effects of 1-methyl-4-phenylpyridinium (MPP(+)) in primary neuron cultures
    A M Marini
    Department of Neurology, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814, USA
    J Neurosci Res 62:814-20. 2000
  7. ncbi request reprint Synaptic deprivation and age-related vulnerability to hypoxic-ischemic neuronal injury. A hypothesis
    A M Marini
    Departments of Neurology and Neuroscience, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA
    Ann N Y Acad Sci 939:238-53. 2001
  8. ncbi request reprint Co-activation of the phosphatidylinositol-3-kinase/Akt signaling pathway by N-methyl-D-aspartate and TrkB receptors in cerebellar granule cell neurons
    D Zhu
    Department of Neurology and Neuroscience, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814, USA
    Amino Acids 23:11-7. 2002
  9. ncbi request reprint Intracellular survival pathways against glutamate receptor agonist excitotoxicity in cultured neurons. Intracellular calcium responses
    A M Marini
    Department of Neurology, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814, USA
    Ann N Y Acad Sci 890:421-37. 1999
  10. ncbi request reprint Genomics and variation of ionotropic glutamate receptors: implications for neuroplasticity
    R H Lipsky
    Sections on Molecular Genetics and Human Genetics, Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland, USA
    Amino Acids 28:169-75. 2005

Collaborators

Detail Information

Publications23

  1. ncbi request reprint Preconditioning and neurotrophins: a model for brain adaptation to seizures, ischemia and other stressful stimuli
    A M Marini
    Department of Neurology and Neuroscience Program, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA
    Amino Acids 32:299-304. 2007
    ....
  2. ncbi request reprint Toward the development of strategies to prevent ischemic neuronal injury. In vitro studies
    A M Marini
    Department of Neurology, Walter Reed Army Medical Center, Washington, DC, USA
    Ann N Y Acad Sci 825:209-19. 1997
    ..NMDA elicited a rapid and time-dependent increase in bFGF mRNA, suggesting that availability of this trophic factor may play a role in the NMDA-mediated neuroprotection...
  3. ncbi request reprint Hormesis: a promising strategy to sustain endogenous neuronal survival pathways against neurodegenerative disorders
    Ann M Marini
    Department of Neurology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA
    Ageing Res Rev 7:21-33. 2008
    ....
  4. ncbi request reprint Brain adaptation to stressful stimuli: a new perspective on potential therapeutic approaches based on BDNF and NMDA receptors
    Ann M Marini
    Department of Neurology and Neuroscience Program, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814, USA
    CNS Neurol Disord Drug Targets 7:382-90. 2008
    ..This mechanism, activation of N-methyl-D-aspartate receptors and its integral relationship with brain-derived neurotrophic factor, may be a critical and general mechanism developed in brain to respond to stressful stimuli...
  5. ncbi request reprint Transient neurologic deficits associated with carbamazepine-induced hypertension
    Ann M Marini
    Department of Neurology and Neuroscience, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, MD 20814, USA
    Clin Neuropharmacol 26:174-6. 2003
    ..A substantial reduction of his carbamazepine dose resulted in the control of his blood pressure and no recurrence of his symptoms...
  6. ncbi request reprint Metabolic effects of 1-methyl-4-phenylpyridinium (MPP(+)) in primary neuron cultures
    A M Marini
    Department of Neurology, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814, USA
    J Neurosci Res 62:814-20. 2000
    ....
  7. ncbi request reprint Synaptic deprivation and age-related vulnerability to hypoxic-ischemic neuronal injury. A hypothesis
    A M Marini
    Departments of Neurology and Neuroscience, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA
    Ann N Y Acad Sci 939:238-53. 2001
    ..Since cerebral infarction is also age related, this hypothesis provides a plausible explanation of how we become more vulnerable to hypoxic-ischemic neuronal injury as a function of age...
  8. ncbi request reprint Co-activation of the phosphatidylinositol-3-kinase/Akt signaling pathway by N-methyl-D-aspartate and TrkB receptors in cerebellar granule cell neurons
    D Zhu
    Department of Neurology and Neuroscience, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814, USA
    Amino Acids 23:11-7. 2002
    ..Therefore, the PI-3 kinase/Akt pathway is co-activated by NMDA and TrkB receptors. The kinetics of BDNF and NMDA-mediated activation of PI-3 kinase/Akt suggests that they have different roles in intraneuronal time-related events...
  9. ncbi request reprint Intracellular survival pathways against glutamate receptor agonist excitotoxicity in cultured neurons. Intracellular calcium responses
    A M Marini
    Department of Neurology, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814, USA
    Ann N Y Acad Sci 890:421-37. 1999
    ..Pretreatment of the cultured neurons with a subtoxic concentration of NMDA, which protects all neurons against the excitotoxic effects of glutamate, did not alter the maximal Ca++[i elicited by an excitotoxic concentration of glutamate...
  10. ncbi request reprint Genomics and variation of ionotropic glutamate receptors: implications for neuroplasticity
    R H Lipsky
    Sections on Molecular Genetics and Human Genetics, Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland, USA
    Amino Acids 28:169-75. 2005
    ....
  11. ncbi request reprint The excitoprotective effect of N-methyl-D-aspartate receptors is mediated by a brain-derived neurotrophic factor autocrine loop in cultured hippocampal neurons
    Xueying Jiang
    Department of Neurology and Division of Neuroscience, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814, USA
    J Neurochem 94:713-22. 2005
    ....
  12. ncbi request reprint AMPA protects cultured neurons against glutamate excitotoxicity through a phosphatidylinositol 3-kinase-dependent activation in extracellular signal-regulated kinase to upregulate BDNF gene expression
    Xuan Wu
    Department of Neurology and Neuroscience, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA
    J Neurochem 90:807-18. 2004
    ..Thus, AMPA receptors protect neurons through a mechanism involving BDNF release, TrkB receptor activation, and a signaling pathway involving a PI3-K dependent activation of MAPK that increases BDNF expression...
  13. pmc N-methyl-D-aspartate and TrkB receptors protect neurons against glutamate excitotoxicity through an extracellular signal-regulated kinase pathway
    Daming Zhu
    Department of Neurology and Neuroscience, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814, USA
    J Neurosci Res 80:104-13. 2005
    ..By increasing antiapoptotic proteins of the Bcl-2 family, NMDA receptor activation may also promote neuronal survival by preventing apoptosis...
  14. ncbi request reprint Role of brain-derived neurotrophic factor and NF-kappaB in neuronal plasticity and survival: From genes to phenotype
    Ann M Marini
    Department of Neurology, Uniformed Services University of the Health Sciences, Bethesda, MD, USA
    Restor Neurol Neurosci 22:121-30. 2004
    ....
  15. ncbi request reprint Inhibition of N-methyl-D-aspartate receptors increases paraoxon-induced apoptosis in cultured neurons
    Xuan Wu
    Department of Neurology, Uniformed Services University of the Health Sciences, Building A, Room 1036, 4301 Jones Bridge Road, Bethesda, MD 20814, USA
    Toxicol Appl Pharmacol 208:57-67. 2005
    ..These results suggest that activation of NMDA receptors protect neurons against paraoxon-induced neurotoxicity by blocking apoptosis initiated by paraoxon...
  16. ncbi request reprint Brain-derived neurotrophic factor in neuronal survival and behavior-related plasticity
    Robert H Lipsky
    Section of Molecular Genetics, Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD 20814, USA
    Ann N Y Acad Sci 1122:130-43. 2007
    ..A better understanding of the influence of BDNF-mediated pathways in cell survival and plasticity will aid in developing new approaches to restoring normal function in disease states...
  17. pmc N-methyl-D-aspartate and TrkB receptor activation in cerebellar granule cells: an in vitro model of preconditioning to stimulate intrinsic survival pathways in neurons
    Xueying Jiang
    Department of Neurology and Neuroscience, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814, USA
    Ann N Y Acad Sci 993:134-45; discussion 159-60. 2003
    ..Thus, crosstalk between these very different receptors provides a rapid means of neuronal communication to upregulate survival proteins through release and transcriptional activation of messenger RNA...
  18. doi request reprint BHLHB2 controls Bdnf promoter 4 activity and neuronal excitability
    Xueying Jiang
    Section on Molecular Genetics, Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Neurosci 28:1118-30. 2008
    ..Together, these results support a role for BHLHB2 as a new modulator of Bdnf transcription and neuronal excitability...
  19. ncbi request reprint Inhibition of protein kinase C protects against paraoxon-mediated neuronal cell death
    Feng Tian
    Department of Neurology and Program in Neuroscience, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA
    Neurotoxicology 28:843-9. 2007
    ..We also show that the pretreatment of Ro-31-8220 blocks paraoxon-induced caspase-3 activity completely. These results suggest that activation of protein kinase C is required for paraoxon neurotoxicity...
  20. pmc Cyclooxygenase-2 inhibition protects cultured cerebellar granule neurons from glutamate-mediated cell death
    Kenneth I Strauss
    Department of Neurosurgery, Temple University School of Medicine, Philadelphia, Pennsylvania 19140, USA
    J Neurotrauma 19:627-38. 2002
    ..These results suggest that glutamate, NMDA, and kainate neurotoxicity involve distinct excitotoxic pathways, and that the glutamate and NMDA pathways may intersect at the level of COX2...
  21. ncbi request reprint Debating the cause of a neurological disorder
    Mark W Duncan
    Science 313:1737. 2006
  22. ncbi request reprint BDNF variation and mood disorders: a novel functional promoter polymorphism and Val66Met are associated with anxiety but have opposing effects
    Xueying Jiang
    Section on Molecular Genetics, Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD 20892, USA
    Neuropsychopharmacology 30:1353-61. 2005
    ..01). Our results suggest that in this population, the low activity -281 A allele may be protective against anxiety and psychiatric morbidity, whereas Met 66 may be a risk allele...
  23. ncbi request reprint Inhibition of protein kinase C promotes neuronal survival in low potassium through an Akt-dependent pathway
    Daming Zhu
    Department of Neurology and Neuroscience, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA
    Neurotox Res 6:281-9. 2004
    ..Because Akt activation appears to be critical in promoting neuronal survival under these culture conditions, increased Akt phosphorylation brought about by inhibiting PKC promotes neuronal survival...