M P Mattson

Summary

Affiliation: University of Kentucky
Country: USA

Publications

  1. ncbi Establishment and plasticity of neuronal polarity
    M P Mattson
    Sanders Brown Research Center on Aging and Department of Anatomy and Neurobiology, University of Kentucky, Lexington 40536 0230, USA
    J Neurosci Res 57:577-89. 1999
  2. ncbi Dietary restriction and 2-deoxyglucose administration improve behavioral outcome and reduce degeneration of dopaminergic neurons in models of Parkinson's disease
    W Duan
    Sanders Brown Research Center on Aging and Department of Anatomy and Neurobiology, University of Kentucky, Lexington, USA
    J Neurosci Res 57:195-206. 1999
  3. ncbi Compartmentalization of signaling in neurons: evolution and deployment
    M P Mattson
    Sanders Brown Research Center on Aging, University of Kentucky, Lexington 40536, USA
    J Neurosci Res 58:2-9. 1999
  4. ncbi Evidence for mitochondrial control of neuronal polarity
    M P Mattson
    Sanders Brown Research Center on Aging and Department of Anatomy and Neurobiology, University of Kentucky, Lexington 40536 0230, USA
    J Neurosci Res 56:8-20. 1999
  5. ncbi Effects of amyloid precursor protein derivatives and oxidative stress on basal forebrain cholinergic systems in Alzheimer's disease
    M P Mattson
    Sanders Brown Research Center on Aging, University of Kentucky, Lexington 40536, USA
    Int J Dev Neurosci 16:737-53. 1998
  6. ncbi "Apoptotic" biochemical cascades in synaptic compartments: roles in adaptive plasticity and neurodegenerative disorders
    M P Mattson
    Sanders Brown Research Center on Aging and Department of Anatomy and Neurobiology, University of Kentucky, Lexington 40536, USA
    J Neurosci Res 58:152-66. 1999
  7. ncbi Amyloid beta-peptide induces apoptosis-related events in synapses and dendrites
    M P Mattson
    Sanders Brown Research Center on Aging and Department of Anatomy and Neurobiology, 211 Sanders Brown Building, University of Kentucky, Lexington, KY 40536, USA
    Brain Res 807:167-76. 1998
  8. ncbi Cell and molecular neurobiology of presenilins: a role for the endoplasmic reticulum in the pathogenesis of Alzheimer's disease?
    M P Mattson
    Sanders Brown Research Center on Aging and Department of Anatomy and Neurobiology, University of Kentucky, Lexington, USA
    J Neurosci Res 50:505-13. 1997
  9. ncbi Cellular signaling roles of TGF beta, TNF alpha and beta APP in brain injury responses and Alzheimer's disease
    M P Mattson
    Sanders Brown Research Center on Aging, University of Kentucky, Lexington 40536 0230, USA
    Brain Res Brain Res Rev 23:47-61. 1997
  10. ncbi Abeta25-35 induces rapid lysis of red blood cells: contrast with Abeta1-42 and examination of underlying mechanisms
    M P Mattson
    Sanders Brown Research Center on Aging and Department of Anatomy and Neurobiology, University of Kentucky, Lexington 40536, USA
    Brain Res 771:147-53. 1997

Collaborators

Detail Information

Publications70

  1. ncbi Establishment and plasticity of neuronal polarity
    M P Mattson
    Sanders Brown Research Center on Aging and Department of Anatomy and Neurobiology, University of Kentucky, Lexington 40536 0230, USA
    J Neurosci Res 57:577-89. 1999
    ..While considerable progress is being made in elucidating mechanisms that regulate neuronal polarity, the seminal event(s) underlying this process remain a mystery. J. Neurosci. Res. 57:577-589...
  2. ncbi Dietary restriction and 2-deoxyglucose administration improve behavioral outcome and reduce degeneration of dopaminergic neurons in models of Parkinson's disease
    W Duan
    Sanders Brown Research Center on Aging and Department of Anatomy and Neurobiology, University of Kentucky, Lexington, USA
    J Neurosci Res 57:195-206. 1999
    ..The striking beneficial effects of DR and 2-DG in models of PD, when considered in light of recent epidemiological data, suggest that DR may prove beneficial in reducing the incidence of PD in humans...
  3. ncbi Compartmentalization of signaling in neurons: evolution and deployment
    M P Mattson
    Sanders Brown Research Center on Aging, University of Kentucky, Lexington 40536, USA
    J Neurosci Res 58:2-9. 1999
    ..The purpose of this introductory article is to set the stage for the following articles by briefly reviewing fundamental aspects of the molecular and cellular biology of synapses in an evolutionary context...
  4. ncbi Evidence for mitochondrial control of neuronal polarity
    M P Mattson
    Sanders Brown Research Center on Aging and Department of Anatomy and Neurobiology, University of Kentucky, Lexington 40536 0230, USA
    J Neurosci Res 56:8-20. 1999
    ....
  5. ncbi Effects of amyloid precursor protein derivatives and oxidative stress on basal forebrain cholinergic systems in Alzheimer's disease
    M P Mattson
    Sanders Brown Research Center on Aging, University of Kentucky, Lexington 40536, USA
    Int J Dev Neurosci 16:737-53. 1998
    ..Knowledge of the cellular and molecular underpinnings of dysfunction and degeneration of cholinergic circuits is leading to the development of novel preventative and therapeutic approaches for Alzheimer's disease and related disorders...
  6. ncbi "Apoptotic" biochemical cascades in synaptic compartments: roles in adaptive plasticity and neurodegenerative disorders
    M P Mattson
    Sanders Brown Research Center on Aging and Department of Anatomy and Neurobiology, University of Kentucky, Lexington 40536, USA
    J Neurosci Res 58:152-66. 1999
    ..We propose that apoptotic cascades function in a continuum in which low levels of activation play roles in adaptive responses to "stressors," whereas higher levels of activation mediate synaptic degeneration and cell death...
  7. ncbi Amyloid beta-peptide induces apoptosis-related events in synapses and dendrites
    M P Mattson
    Sanders Brown Research Center on Aging and Department of Anatomy and Neurobiology, 211 Sanders Brown Building, University of Kentucky, Lexington, KY 40536, USA
    Brain Res 807:167-76. 1998
    ..Collectively, the data demonstrate that apoptotic biochemical cascades can be activated in synapses and dendrites by Abeta, and suggest that such 'synaptic apoptosis' may contribute to synaptic dysfunction and degeneration in AD...
  8. ncbi Cell and molecular neurobiology of presenilins: a role for the endoplasmic reticulum in the pathogenesis of Alzheimer's disease?
    M P Mattson
    Sanders Brown Research Center on Aging and Department of Anatomy and Neurobiology, University of Kentucky, Lexington, USA
    J Neurosci Res 50:505-13. 1997
    ..Collectively, the emerging data suggest intriguing roles of PSs in neuronal plasticity and cell death and highlight the importance of the ER as a regulatory site involved in the pathogenesis of neuronal degeneration in AD...
  9. ncbi Cellular signaling roles of TGF beta, TNF alpha and beta APP in brain injury responses and Alzheimer's disease
    M P Mattson
    Sanders Brown Research Center on Aging, University of Kentucky, Lexington 40536 0230, USA
    Brain Res Brain Res Rev 23:47-61. 1997
    ..Knowledge of these signaling pathways is revealing novel molecular targets on which to focus neuroprotective therapeutic strategies in disorders ranging from stroke to Alzheimer's disease...
  10. ncbi Abeta25-35 induces rapid lysis of red blood cells: contrast with Abeta1-42 and examination of underlying mechanisms
    M P Mattson
    Sanders Brown Research Center on Aging and Department of Anatomy and Neurobiology, University of Kentucky, Lexington 40536, USA
    Brain Res 771:147-53. 1997
    ....
  11. ncbi Anti-death properties of TNF against metabolic poisoning: mitochondrial stabilization by MnSOD
    A J Bruce-Keller
    Sanders Brown Research Center on Aging, Department of Anatomy and Neurobiology, University of Kentucky, Lexington 40536 0230, USA
    J Neuroimmunol 93:53-71. 1999
    ..Additional studies showed that levels of oxidative stress and striatal lesion size following 3-NP administration in vivo are increased in mice lacking TNF receptors...
  12. pmc Neurotrophic factors [activity-dependent neurotrophic factor (ADNF) and basic fibroblast growth factor (bFGF)] interrupt excitotoxic neurodegenerative cascades promoted by a PS1 mutation
    Q Guo
    Sanders Brown Research Center on Aging and Department of Anatomy and Neurobiology, University of Kentucky, Lexington, KY 40536, USA
    Proc Natl Acad Sci U S A 96:4125-30. 1999
    ..Our data indicate that neurotrophic factors can interrupt excitotoxic neurodegenerative cascades promoted by PS1 mutations...
  13. ncbi Increased vulnerability of hippocampal neurons from presenilin-1 mutant knock-in mice to amyloid beta-peptide toxicity: central roles of superoxide production and caspase activation
    Q Guo
    Sanders Brown Research Center on Aging and Department of Anatomy and Neurobiology, University of Kentucky, Lexington 40536 0230, USA
    J Neurochem 72:1019-29. 1999
    ..Increased oxidative stress may contribute to the pathogenic action of PS1 mutations, and antioxidants may counteract the adverse property of such AD-linked mutations...
  14. ncbi Altered calcium homeostasis and mitochondrial dysfunction in cortical synaptic compartments of presenilin-1 mutant mice
    J G Begley
    Sanders Brown Research Center on Aging and Department of Anatomy and Neurobiology, University of Kentucky, Lexington 40536 0230, USA
    J Neurochem 72:1030-9. 1999
    ..Abnormal synaptic calcium homeostasis and mitochondrial dysfunction may contribute to the pathogenic mechanism of presenilin-1 mutations...
  15. ncbi ALS-linked Cu/Zn-SOD mutation increases vulnerability of motor neurons to excitotoxicity by a mechanism involving increased oxidative stress and perturbed calcium homeostasis
    I I Kruman
    Sanders Brown Research Center on Aging, University of Kentucky, Lexington 40536, USA
    Exp Neurol 160:28-39. 1999
    ..The mitochondrial dysfunction associated with Cu/Zn-SOD mutations may play an important role in disturbing calcium homeostasis and increasing oxyradical production, thereby increasing the vulnerability of MNs to excitotoxicity...
  16. ncbi The prostate apoptosis response-4 protein participates in motor neuron degeneration in amyotrophic lateral sclerosis
    W A Pedersen
    Sanders Brown Research Center on Aging, Department of Neurology, and Department of Anatomy and Neurobiology, University of Kentucky, Lexington, Kentucky 40536, USA
    FASEB J 14:913-24. 2000
    ..Collectively, these data suggest a role for Par-4 in models of motor neuron injury relevant to ALS...
  17. ncbi Elevated hepatic and depressed renal cytochrome P450 activity in the Tg2576 transgenic mouse model of Alzheimer's disease
    P J Van Ess
    College of Pharmacy, Division of Pharmaceutical Sciences, University of Kentucky, Lexington, Kentucky, USA
    J Neurochem 80:571-8. 2002
    ..The presence of the mutant hAPP protein was detected in the brain, kidney and livers of tg(hAPP) mice...
  18. ncbi Neuroprotective role for the p50 subunit of NF-kappaB in an experimental model of Huntington's disease
    Z Yu
    Sanders Brown Research Center on Aging, National Institute on Aging Gerontology Research Center, Baltimore, MD 21224, USA
    J Mol Neurosci 15:31-44. 2000
    ..Cultured striatal neurons from p50-/- mice exhibited enhanced oxidative stress, perturbed calcium regulation, and increased cell death following exposure to 3NP, suggesting a direct adverse effect of p50 deficiency in striatal neurons...
  19. ncbi Pivotal role for acidic sphingomyelinase in cerebral ischemia-induced ceramide and cytokine production, and neuronal apoptosis
    Z F Yu
    Sanders Brown Research Center on Aging, University of Kentucky, Lexington 40536, USA
    J Mol Neurosci 15:85-97. 2000
    ....
  20. ncbi Presenilin-1 mutations increase levels of ryanodine receptors and calcium release in PC12 cells and cortical neurons
    S L Chan
    Sanders Brown Research Center on Aging, University of Kentucky, Lexington, Kentucky 40536, USA
    J Biol Chem 275:18195-200. 2000
    ....
  21. pmc Evidence that Par-4 participates in the pathogenesis of HIV encephalitis
    I I Kruman
    Sanders Brown Research Center on Aging, Department of Neurology, Lexington, Kentucky, USA
    Am J Pathol 155:39-46. 1999
    ....
  22. ncbi Nicotine attenuates arachidonic acid-induced overexpression of nitric oxide synthase in cultured spinal cord neurons
    M Toborek
    Department of Surgery, University of Kentucky, Lexington, Kentucky, 40536, USA
    Exp Neurol 161:609-20. 2000
    ..In addition, nicotine can exert a neuroprotective effect by attenuation of AA-induced upregulation of nNOS metabolism. These data may have therapeutic implications for the treatment of acute spinal cord trauma...
  23. ncbi Par-4 is a mediator of neuronal degeneration associated with the pathogenesis of Alzheimer disease
    Q Guo
    Sanders Brown Research Center on Aging, University of Kentucky, Lexington 40536, USA
    Nat Med 4:957-62. 1998
    ..Par-4 expression was enhanced, and mitochondrial dysfunction and apoptosis exacerbated, in cells expressing presenilin-1 mutations associated with early-onset inherited AD...
  24. ncbi ALS-linked Cu/Zn-SOD mutation impairs cerebral synaptic glucose and glutamate transport and exacerbates ischemic brain injury
    Z Guo
    Sanders Brown Research Center on Aging, University of Kentucky, Lexington, USA
    J Cereb Blood Flow Metab 20:463-8. 2000
    ..Moreover, our data demonstrate a direct adverse effect of the mutant enzyme on synaptic function...
  25. ncbi Lack of the p50 subunit of nuclear factor-kappaB increases the vulnerability of hippocampal neurons to excitotoxic injury
    Z Yu
    Sanders Brown Research Center on Aging, University of Kentucky, Lexington, Kentucky 40536, USA
    J Neurosci 19:8856-65. 1999
    ..Collectively, our data demonstrate an important role for the p50 subunit of NF-kappaB in protecting neurons against excitotoxic cell death...
  26. ncbi Presenilin-1 mutation increases neuronal vulnerability to focal ischemia in vivo and to hypoxia and glucose deprivation in cell culture: involvement of perturbed calcium homeostasis
    M P Mattson
    Sanders Brown Research Center on Aging, Department of Anatomy, University of Kentucky, Lexington, Kentucky 40536, USA
    J Neurosci 20:1358-64. 2000
    ..The data further suggest that drugs that stabilize endoplasmic reticulum calcium homeostasis may prove effective in suppressing the neurodegenerative process in AD patients...
  27. ncbi Roles of nuclear factor kappaB in neuronal survival and plasticity
    M P Mattson
    Sanders Brown Research Center on Aging and Department of Anatomy and Neurobiology, University of Kentucky, Lexington, USA
    J Neurochem 74:443-56. 2000
    ....
  28. ncbi Increased vulnerability of hippocampal neurons to excitotoxic necrosis in presenilin-1 mutant knock-in mice
    Q Guo
    Sanders Brown Research Center on Aging and Department of Anatomy and Neurobiology, University of Kentucky, Lexington 40536, USA
    Nat Med 5:101-6. 1999
    ..These findings establish a direct link between a genetic defect that causes AD and excitotoxic neuronal degeneration, and indicate new avenues for therapeutic intervention in AD patients...
  29. ncbi Dietary restriction protects hippocampal neurons against the death-promoting action of a presenilin-1 mutation
    H Zhu
    Department of Anatomy and Neurobiology, Sanders Brown Research Center on Aging, University of Kentucky, 211 Sanders Brown Building, 800 South Limestone Street, Lexington, KY 40536, USA
    Brain Res 842:224-9. 1999
    ..These findings indicate that the neurodegeneration-promoting effect of an AD-linked mutation is subject to modification by diet...
  30. ncbi Effects of NF-kappaB1 (p50) targeted gene disruption on ionizing radiation-induced NF-kappaB activation and TNFalpha, IL-1alpha, IL-1beta and IL-6 mRNA expression in vivo
    D Zhou
    Division of Allergy, Immunology and Rheumatology, Department of Internal Medicine, University of Kentucky, Lexington, KY 40536, USA
    Int J Radiat Biol 77:763-72. 2001
    ..To investigate the role of the NF-kappaB1 (p50) gene in ionizing radiation (IR)-induced NF-kappaB activation and TNFalpha, IL-1alpha, IL-1beta and IL-6 mRNA expression in vivo...
  31. ncbi Exacerbation of damage and altered NF-kappaB activation in mice lacking tumor necrosis factor receptors after traumatic brain injury
    P G Sullivan
    Sanders Brown Center on Aging, University of Kentucky, Lexington, Kentucky 40536 0230, USA
    J Neurosci 19:6248-56. 1999
    ..Analysis of NF-kappaB activation and relative levels of MnSOD revealed delayed responses in the injured cortex of TNFR-KO animals compared with wild-type animals, implying that endogenous TNFalpha may be neuroprotective after TBI...
  32. ncbi Oxidized lipoproteins increase reactive oxygen species formation in microglia and astrocyte cell lines
    J N Keller
    Sanders Brown Center on Aging, University of Kentucky, 101 Sanders Brown Building, Lexington, KY, 40536 0230, USA
    Brain Res 830:10-5. 1999
    ....
  33. ncbi Antiinflammatory effects of estrogen on microglial activation
    A J Bruce-Keller
    Department of Anatomy and Neurobiology, University of Kentucky, Lexington 40536, USA
    Endocrinology 141:3646-56. 2000
    ..These results describe a novel mechanism by which estrogen may attenuate the progression of neurodegenerative disease and suggest new pathways for therapeutic intervention in clinical settings...
  34. ncbi HIV-1 protein Tat induces apoptosis of hippocampal neurons by a mechanism involving caspase activation, calcium overload, and oxidative stress
    I I Kruman
    Department of Anatomy and Neurobiology, University of Kentucky, Lexington, Kentucky, 40536, USA
    Exp Neurol 154:276-88. 1998
    ..Agents that interupt this apoptotic cascade may prove beneficial in preventing neuronal degeneration and associated dementia in AIDS patients...
  35. ncbi Nicotine protects against arachidonic-acid-induced caspase activation, cytochrome c release and apoptosis of cultured spinal cord neurons
    R Garrido
    Department of Surgery, University of Kentucky Medical Center, Lexington, Kentucky, USA
    J Neurochem 76:1395-403. 2001
    ..These results indicate that nicotine can exert potent neuroprotective effects by inhibiting arachidonic acid induced apoptotic cascades of spinal cord neurons...
  36. pmc Estrogen protects against the synergistic toxicity by HIV proteins, methamphetamine and cocaine
    J Turchan
    Department of Neurology, University of Kentucky, Lexington, USA
    BMC Neurosci 2:3. 2001
    ..We determined the combined effects of dopaminergic drugs, methamphetamine, or cocaine with neurotoxic HIV proteins, gp120 and Tat...
  37. ncbi Lysophosphatidic acid induction of neuronal apoptosis and necrosis
    M R Steiner
    Department of Microbiology and Immunology, University of Kentucky, Lexington 40536, USA
    Ann N Y Acad Sci 905:132-41. 2000
    ..Thus, LPA-induced neuronal apoptosis is associated with mitochondrial alterations, the generation of reactive oxygen species and nitric oxide, and protection by pretreatment with a serum constituent, insulin-like growth factor 1...
  38. ncbi Altered neuronal and microglial responses to excitotoxic and ischemic brain injury in mice lacking TNF receptors
    A J Bruce
    Sanders Brown Research Center on Aging, University of Kentucky, Lexington 40536 0230, USA
    Nat Med 2:788-94. 1996
    ..Drugs that target TNF signaling pathways may prove beneficial in treating stroke and traumatic brain injury...
  39. ncbi Molecular functionalization of carbon nanotubes and use as substrates for neuronal growth
    M P Mattson
    Sanders Brown Research Center on Aging and Department of Anatomy and Neurobiology, University of Kentucky, Lexington 40536, USA
    J Mol Neurosci 14:175-82. 2000
    ..These findings establish the feasability of using nanotubes as substrates for nerve cell growth and as probes of neuronal function at the nanometer scale...
  40. ncbi Horizontal cell electrical coupling in the giant danio: synaptic modulation by dopamine and synaptic maintenance by calcium
    D G McMahon
    Department of Physiology, University of Kentucky, Lexington 40536 0084, USA
    Brain Res 718:89-96. 1996
    ..The effects of calcium on synaptic maintenance may be related to structural changes observed in horizontal cell electrical synapses during light adaptation...
  41. ncbi Cytochrome P450 and antioxidant activity in interleukin-6 knockout mice after induction of the acute-phase response
    G W Warren
    Graduate Center for Toxicology, University of Kentucky, Lexington, KY 40536 0082, USA
    J Interferon Cytokine Res 21:821-6. 2001
    ..These results support IL-6 as a critical mediator of the effects of LPS on specific hepatic and renal CYP activities and hepatic CAT activity...
  42. pmc Capacitative calcium entry deficits and elevated luminal calcium content in mutant presenilin-1 knockin mice
    M A Leissring
    Laboratory of Molecular Neuropathogenesis, Department of Neurobiology and Behavior, Center for the Neurobiology of Learning and Memory and Institute for Brain Aging and Dementia, University of California Irvine 92697 4561, USA
    J Cell Biol 149:793-8. 2000
    ..Collectively, our findings suggest that the overfilling of calcium stores represents the fundamental cellular defect underlying the alterations in calcium signaling conferred by presenilin mutations...
  43. ncbi AMP-activated protein kinase is highly expressed in neurons in the developing rat brain and promotes neuronal survival following glucose deprivation
    C Culmsee
    Laboratory of Neurosciences, National Institute on Aging, Baltimore, MD 21224, USA
    J Mol Neurosci 17:45-58. 2001
    ..These findings suggest that AMPK can protect neurons against metabolic and excitotoxic insults relevant to the pathogenesis of several different neurodegenerative conditions...
  44. ncbi Telomerase protects developing neurons against DNA damage-induced cell death
    C Lu
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Brain Res Dev Brain Res 131:167-71. 2001
    ..Emerging findings suggest that DNA damage may trigger the death of neurons during brain development and in neurodegenerative disorders. Our data therefore suggest roles for TERT in modulating such cell deaths...
  45. ncbi p38 MAP kinase mediates nitric oxide-induced apoptosis of neural progenitor cells
    A Cheng
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, Baltimore, Maryland 21224, USA
    J Biol Chem 276:43320-7. 2001
    ..The ability of nitric oxide to trigger death of NPC by a mechanism involving p38 MAP kinase suggests that this diffusible gas may regulate NPC fate in physiological and pathological settings in which NO is produced...
  46. ncbi Calsenilin enhances apoptosis by altering endoplasmic reticulum calcium signaling
    C Lilliehook
    Laboratory of Molecular Neuropsychiatry, Department of Psychiatry, Mount Sinai School of Medicine, New York, New York 10029, USA
    Mol Cell Neurosci 19:552-9. 2002
    ..Taken together, these data suggest that calsenilin causes cells to be more susceptible to apoptotic triggers, possibly by altering calcium dynamics...
  47. ncbi Nerve growth factor survival signaling in cultured hippocampal neurons is mediated through TrkA and requires the common neurotrophin receptor P75
    C Culmsee
    Institut fur Pharmakologie und Toxikologie, Philipps Universitat Marburg, Ketzerbach 63, 35032, Marburg, Germany
    Neuroscience 115:1089-108. 2002
    ..Overall, our results indicate an essential role for p75NTR in supporting NGF-triggered TrkA signaling pathways mediating neuronal survival in hippocampal neurons...
  48. ncbi Heterogeneity of endocytic proteins: distribution of clathrin adaptor proteins in neurons and glia
    P J Yao
    Laboratory of Neurosciences, Gerontology Research Center, NIA NIH, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Neuroscience 121:25-37. 2003
    ..The findings also provide information on the distribution of AP2, CALM, and epsin 1 in cells of the nervous system that suggest different roles for these endocytic proteins in the biology of these cells...
  49. ncbi Cell death in HIV dementia
    M P Mattson
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Cell Death Differ 12:893-904. 2005
    ..Drugs and diets that target oxidative stress, excitotoxicity, inflammation and lipid metabolism are in development for the treatment of HIV-1 patients...
  50. ncbi Molecular and cellular mechanisms of neuronal cell death in HIV dementia
    W Li
    RT Johnson Division of Neuroimmunology and Neurological Infection, Department of Neurology, Johns Hopkins University, Baltimore, MD 21287, USA
    Neurotox Res 8:119-34. 2005
    ....
  51. ncbi Roles for NF-kappaB in nerve cell survival, plasticity, and disease
    M P Mattson
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA
    Cell Death Differ 13:852-60. 2006
    ..Molecular pathways upstream and downstream of NF-kappaB in neurons are being elucidated and may provide novel targets for therapeutic intervention in various neurological disorders...
  52. ncbi 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
    ....
  53. pmc DNA damage responses in neural cells: Focus on the telomere
    P Zhang
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Neuroscience 145:1439-48. 2007
    ..Indeed, work in this and other laboratories has shown that dietary folic acid can protect neurons against Alzheimer's disease by keeping homocysteine levels low and thereby minimizing the misincorporation of uracil into DNA in neurons...
  54. ncbi Selective and biphasic effect of the membrane lipid peroxidation product 4-hydroxy-2,3-nonenal on N-methyl-D-aspartate channels
    C Lu
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, Baltimore 21224, USA
    J Neurochem 78:577-89. 2001
    ..These findings show that the membrane lipid peroxidation product 4HN can modulate NMDA channel activity, suggesting a role for this aldehyde in physiological and pathophysiological responses of neurons to oxidative stress...
  55. ncbi HIV-1 Tat through phosphorylation of NMDA receptors potentiates glutamate excitotoxicity
    N J Haughey
    Laboratory of Neurosciences, National Institute on Aging, Baltimore, Maryland, USA
    J Neurochem 78:457-67. 2001
    ..Together, these findings suggest that NMDA receptors play an important role in Tat neurotoxicity and the mechanisms identified may provide additional therapeutic targets for the treatment of HIV-1 associated dementia...
  56. ncbi Brain-derived neurotrophic factor mediates an excitoprotective effect of dietary restriction in mice
    W Duan
    Laboratory of Neurosciences, National Institute on Aging, Baltimore, Maryland 21224, USA
    J Neurochem 76:619-26. 2001
    ..These results bolster accumulating evidence that DR may be an effective approach for increasing the resistance of the brain to damage and enhancing brain neuronal plasticity...
  57. ncbi Microglial activation resulting from CD40-CD40L interaction after beta-amyloid stimulation
    J Tan
    The Roskamp Institute, University of South Florida, 3515 East Fletcher Avenue, Tampa, FL 33613, USA
    Science 286:2352-5. 1999
    ..Finally, abnormal tau phosphorylation was reduced in Tg APPsw animals deficient for CD40L, suggesting that the CD40-CD40L interaction is an early event in AD pathogenesis...
  58. ncbi Integrin signaling via the PI3-kinase-Akt pathway increases neuronal resistance to glutamate-induced apoptosis
    D S Gary
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, Baltimore, Maryland 21224, USA
    J Neurochem 76:1485-96. 2001
    ..The ability of integrin-mediated signaling to prevent glutamate-induced apoptosis suggests a mechanism whereby neuron-substrate interactions can promote neuron survival under conditions of glutamate receptor overactivation...
  59. ncbi Hippocampal neurons of mice deficient in DNA-dependent protein kinase exhibit increased vulnerability to DNA damage, oxidative stress and excitotoxicity
    C Culmsee
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Brain Res Mol Brain Res 87:257-62. 2001
    ..Our results suggest that DNA-PK activity is important for neuron survival under conditions that may occur in neurological disorders...
  60. ncbi A synthetic inhibitor of p53 protects neurons against death induced by ischemic and excitotoxic insults, and amyloid beta-peptide
    C Culmsee
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, Baltimore 21224, USA
    J Neurochem 77:220-8. 2001
    ....
  61. ncbi Caspase-mediated suppression of glutamate (AMPA) receptor channel activity in hippocampal neurons in response to DNA damage promotes apoptosis and prevents necrosis: implications for neurological side effects of cancer therapy and neurodegenerative disord
    C Lu
    Laboratory of Neurosciences, National Institute on Aging, 5600 Nathan Shock Drive, Baltimore, Maryland 21224, USA
    Neurobiol Dis 8:194-206. 2001
    ..These findings have important implications for treatment of patients with cancer and neurodegenerative disorders...
  62. ncbi Endoplasmic reticulum D-myo-inositol 1,4,5-trisphosphate-sensitive stores regulate nuclear factor-kappaB binding activity in a calcium-independent manner
    G W Glazner
    Laboratory of Neurosciences, NIA Gerontology Research Center, National Institutes of Health, Baltimore, Maryland 21224, USA
    J Biol Chem 276:22461-7. 2001
    ....
  63. ncbi Emerging roles for telomerase in regulating cell differentiation and survival: a neuroscientist's perspective
    M P Mattson
    Laboratory of Neurosciences 4F02, National Institute on Aging Gerontology Research Center, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Mech Ageing Dev 122:659-71. 2001
    ....
  64. ncbi Evidence for the involvement of Par-4 in ischemic neuron cell death
    C Culmsee
    Laboratory of Neurosciences, National Institute on Aging, Baltimore, Maryland 21224, USA
    J Cereb Blood Flow Metab 21:334-43. 2001
    ..The current data suggest that early up-regulation of Par-4 plays a pivotal role in ischemic neuronal death in animal models of stroke and cardiac arrest...
  65. ncbi Dietary restriction stimulates BDNF production in the brain and thereby protects neurons against excitotoxic injury
    W Duan
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, Baltimore, MD 21224, USA
    J Mol Neurosci 16:1-12. 2001
    ....
  66. ncbi Dimethyl sulfoxide suppresses NMDA- and AMPA-induced ion currents and calcium influx and protects against excitotoxic death in hippocampal neurons
    C Lu
    Laboratory of Neurosciences, Gerontology Research Center 4F01, National Institute on Aging, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Exp Neurol 170:180-5. 2001
    ..Our data also identify a mechanism that might explain clinical effects of DMSO on both peripheral and CNS neurons and suggest a potential use for DMSO in the treatment of excitotoxic neurodegenerative conditions...
  67. ncbi Corticotropin-releasing hormone protects neurons against insults relevant to the pathogenesis of Alzheimer's disease
    W A Pedersen
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, Baltimore, Maryland 21224, USA
    Neurobiol Dis 8:492-503. 2001
    ..Our results suggest that disturbances in HPA axis function can occur independently of alterations in CRH mRNA levels in Alzheimer's disease brain and further suggest an additional role for CRH in protecting neurons against cell death...
  68. pmc Neuroprotective effects of gelsolin during murine stroke
    M Endres
    Stroke and Neurovascular Regulation, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA
    J Clin Invest 103:347-54. 1999
    ..Hence, enhancement or mimicry of gelsolin activity may be neuroprotective during stroke...
  69. ncbi Amyloid beta-peptide activates nuclear factor-kappaB through an N-methyl-D-aspartate signaling pathway in cultured cerebellar cells
    E M Kawamoto
    Department of Pharmacology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil
    J Neurosci Res 86:845-60. 2008
    ..Collectively, these findings suggest that A beta activates NF-kappaB by an NMDA-Src-Ras-like protein through MAPK and PI3-k pathways in cultured cerebellar cells. This pathway may mediate an adaptive, neuroprotective response to A beta...