Mark P Mattson

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. ncbi request reprint Brain evolution and lifespan regulation: conservation of signal transduction pathways that regulate energy metabolism
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center 4F01, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Mech Ageing Dev 123:947-53. 2002
  2. pmc Enhancing the GLP-1 receptor signaling pathway leads to proliferation and neuroprotection in human neuroblastoma cells
    Yazhou Li
    Drug Design and Development Section, Laboratory of Neurosciences, Intramural Research Program, National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224, USA
    J Neurochem 113:1621-31. 2010
  3. pmc Interrogation of brain miRNA and mRNA expression profiles reveals a molecular regulatory network that is perturbed by mutant huntingtin
    Jing Jin
    Division of Neurobiology, Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    J Neurochem 123:477-90. 2012
  4. pmc Exendin-4 ameliorates motor neuron degeneration in cellular and animal models of amyotrophic lateral sclerosis
    Yazhou Li
    Laboratory of Neurosciences, Intramural Research Program, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, United States of America
    PLoS ONE 7:e32008. 2012
  5. pmc Molecular changes in brain aging and Alzheimer's disease are mirrored in experimentally silenced cortical neuron networks
    Marc Gleichmann
    Laboratory of Neurosciences, National Institute on Aging, Intramural Research Program, Biomedical Research Center, Baltimore, MD 21224, USA
    Neurobiol Aging 33:205.e1-18. 2012
  6. pmc 3xTgAD mice exhibit altered behavior and elevated Aβ after chronic mild social stress
    Sarah M Rothman
    Laboratory of Neurosciences, National Institute on Aging, Intramural Research Program, National Institutes of Health, Baltimore, MD 21224, USA
    Neurobiol Aging 33:830.e1-12. 2012
  7. pmc TLR2 activation inhibits embryonic neural progenitor cell proliferation
    Eitan Okun
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, Maryland 21224, USA
    J Neurochem 114:462-74. 2010
  8. ncbi request reprint TRF2 dysfunction elicits DNA damage responses associated with senescence in proliferating neural cells and differentiation of neurons
    Peisu Zhang
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA
    J Neurochem 97:567-81. 2006
  9. ncbi request reprint Numb modifies neuronal vulnerability to amyloid beta-peptide in an isoform-specific manner by a mechanism involving altered calcium homeostasis: implications for neuronal death in Alzheimer's disease
    Sic L Chan
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, Baltimore, MD 21224, USA
    Neuromolecular Med 1:55-67. 2002
  10. ncbi request reprint Neuronal expression of familial Parkinson's disease A53T α-synuclein causes early motor impairment, reduced anxiety and potential sleep disturbances in mice
    Sarah M Rothman
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, National Institutes of Health, Baltimore, MD 21224, USA
    J Parkinsons Dis 3:215-29. 2013

Collaborators

Detail Information

Publications161 found, 100 shown here

  1. ncbi request reprint Brain evolution and lifespan regulation: conservation of signal transduction pathways that regulate energy metabolism
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center 4F01, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Mech Ageing Dev 123:947-53. 2002
    ..Thus a prominent evolutionarily conserved function of the nervous system is to regulate food acquisition and energy metabolism, thereby controlling lifespan...
  2. pmc Enhancing the GLP-1 receptor signaling pathway leads to proliferation and neuroprotection in human neuroblastoma cells
    Yazhou Li
    Drug Design and Development Section, Laboratory of Neurosciences, Intramural Research Program, National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224, USA
    J Neurochem 113:1621-31. 2010
    ....
  3. pmc Interrogation of brain miRNA and mRNA expression profiles reveals a molecular regulatory network that is perturbed by mutant huntingtin
    Jing Jin
    Division of Neurobiology, Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    J Neurochem 123:477-90. 2012
    ....
  4. pmc Exendin-4 ameliorates motor neuron degeneration in cellular and animal models of amyotrophic lateral sclerosis
    Yazhou Li
    Laboratory of Neurosciences, Intramural Research Program, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, United States of America
    PLoS ONE 7:e32008. 2012
    ..Together, our results suggest that GLP-1 receptor agonists warrant further evaluation to assess whether their neuroprotective potential is of therapeutic relevance in ALS...
  5. pmc Molecular changes in brain aging and Alzheimer's disease are mirrored in experimentally silenced cortical neuron networks
    Marc Gleichmann
    Laboratory of Neurosciences, National Institute on Aging, Intramural Research Program, Biomedical Research Center, Baltimore, MD 21224, USA
    Neurobiol Aging 33:205.e1-18. 2012
    ..Our findings suggest that reduced inhibitory neurotransmission during aging and in AD may be the result of compensatory responses that, paradoxically, render the neurons vulnerable to Ca(2+)-mediated degeneration...
  6. pmc 3xTgAD mice exhibit altered behavior and elevated Aβ after chronic mild social stress
    Sarah M Rothman
    Laboratory of Neurosciences, National Institute on Aging, Intramural Research Program, National Institutes of Health, Baltimore, MD 21224, USA
    Neurobiol Aging 33:830.e1-12. 2012
    ..Findings suggest 3xTgAD mice are more vulnerable than control mice to chronic psychosocial stress, and that such chronic stress exacerbates Aβ accumulation and impairs neurotrophic signaling...
  7. pmc TLR2 activation inhibits embryonic neural progenitor cell proliferation
    Eitan Okun
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, Maryland 21224, USA
    J Neurochem 114:462-74. 2010
    ..TLR2-mediated inhibition of NPC proliferation may therefore be a mechanism by which infection, ischemia, and inflammation adversely affect brain development...
  8. ncbi request reprint TRF2 dysfunction elicits DNA damage responses associated with senescence in proliferating neural cells and differentiation of neurons
    Peisu Zhang
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA
    J Neurochem 97:567-81. 2006
    ....
  9. ncbi request reprint Numb modifies neuronal vulnerability to amyloid beta-peptide in an isoform-specific manner by a mechanism involving altered calcium homeostasis: implications for neuronal death in Alzheimer's disease
    Sic L Chan
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, Baltimore, MD 21224, USA
    Neuromolecular Med 1:55-67. 2002
    ..Our findings also suggest that the effects of Numb on cell fate decisions, both during development of the nervous system and in neurodegenertive disorders, are mediated by changes in cellular calcium homeostasis...
  10. ncbi request reprint Neuronal expression of familial Parkinson's disease A53T α-synuclein causes early motor impairment, reduced anxiety and potential sleep disturbances in mice
    Sarah M Rothman
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, National Institutes of Health, Baltimore, MD 21224, USA
    J Parkinsons Dis 3:215-29. 2013
    ..Mutations in the human α-synuclein gene lead to early-onset Parkinson's disease (PD); however, phenotypes of α-synuclein mutant mice vary depending upon the promoter driving transgene expression...
  11. pmc Naphthazarin protects against glutamate-induced neuronal death via activation of the Nrf2/ARE pathway
    Tae Gen Son
    Laboratory of Neurosciences, National Institute on Aging, Intramural Research Program, 251 Bayview Blvd, Baltimore, MD 21224, USA
    Biochem Biophys Res Commun 433:602-6. 2013
    ....
  12. pmc Brain-derived neurotrophic factor as a regulator of systemic and brain energy metabolism and cardiovascular health
    Sarah M Rothman
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, National Institutes of Health, Baltimore, Maryland 21224, USA
    Ann N Y Acad Sci 1264:49-63. 2012
    ..Collectively, findings reviewed in this paper provide a rationale for targeting BDNF signaling for novel therapeutic interventions in a range of metabolic and neurological disorders...
  13. pmc Ceruloplasmin deficiency results in an anxiety phenotype involving deficits in hippocampal iron, serotonin, and BDNF
    Sarah J Texel
    Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    J Neurochem 120:125-34. 2012
    ..Thus, Cp deficiency causes an anxiety phenotype by a mechanism that involves decreased levels of iron, 5HT, NE, and BDNF in the hippocampus...
  14. ncbi request reprint Presenilin-1 mutations sensitize neurons to DNA damage-induced death by a mechanism involving perturbed calcium homeostasis and activation of calpains and caspase-12
    Sic L Chan
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, Baltimore, Maryland 21224, USA
    Neurobiol Dis 11:2-19. 2002
    ..Agents that release Ca(2+) from the ER increased the vulnerability of cells expressing mutant PS1 to DNA damage. By promoting ER-mediated apoptotic proteolytic cascades, PS1 mutations may sensitize neurons to DNA damage...
  15. ncbi request reprint Membrane properties of rat embryonic multipotent neural stem cells
    Jingli Cai
    Laboratory of Neurosciences, Gerontology Research Center, National Institute on Aging, Baltimore, Maryland 21224, USA
    J Neurochem 88:212-26. 2004
    ..Overall, our results show that fetal NSCs exhibit a unique signature that can be used to determine their location and assess their ability to respond to their environment...
  16. doi request reprint Modulation of DNA base excision repair during neuronal differentiation
    Peter Sykora
    Laboratory of Molecular Gerontology, National Institute on Aging National Institutes of Health, Baltimore, MD, USA
    Neurobiol Aging 34:1717-27. 2013
    ..Thus, because of their higher BER capacity, proliferative neural progenitor cells are more efficient at repairing DNA damage compared with their neuronally differentiated progeny...
  17. pmc Mitochondrial superoxide production negatively regulates neural progenitor proliferation and cerebral cortical development
    Yan Hou
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA
    Stem Cells 30:2535-47. 2012
    ..Taken together, our findings suggest that mitochondrial SO flashes negatively regulate NPC self-renewal in the developing cerebral cortex...
  18. pmc Involvement of PGC-1α in the formation and maintenance of neuronal dendritic spines
    Aiwu Cheng
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, Maryland 21224, USA
    Nat Commun 3:1250. 2012
    ..Our findings suggest that proliferator-activated receptor γ co-activator-1α and mitochondrial biogenesis have important roles in the formation and maintenance of hippocampal dendritic spines and synapses...
  19. pmc Plumbagin, a novel Nrf2/ARE activator, protects against cerebral ischemia
    Tae Gen Son
    Laboratory of Neurosciences, National Institute on Aging, Intramural Research Program, Baltimore, MD 21224, USA
    J Neurochem 112:1316-26. 2010
    ..Our findings establish precedence for the identification and characterization of neuroprotective phytochemicals based upon their ability to activate adaptive cellular stress response pathways...
  20. pmc Hippocampal gene expression patterns underlying the enhancement of memory by running in aged mice
    Alexis M Stranahan
    Cellular and Molecular Neuroscience Section, Laboratory of Neurosciences, National Institute on Aging, Biomedical Research Center, 251 Bayview Boulevard, Baltimore, MD 21224 6825, United States
    Neurobiol Aging 31:1937-49. 2010
    ..These results suggest that the enhancement of cognitive function by lifelong exercise is associated with an altered transcriptional profile following learning...
  21. pmc Evidence that OGG1 glycosylase protects neurons against oxidative DNA damage and cell death under ischemic conditions
    Dong Liu
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, Maryland 21224, USA
    J Cereb Blood Flow Metab 31:680-92. 2011
    ..Thus, OGG1 has a pivotal role in repairing oxidative damage to nuclear DNA under ischemic conditions, thereby reducing brain damage and improving functional outcome...
  22. pmc Diet-induced elevations in serum cholesterol are associated with alterations in hippocampal lipid metabolism and increased oxidative stress
    Alexis M Stranahan
    Cellular and Molecular Neuroscience Section, Laboratory of Neurosciences, National Institute on Aging, Biomedical Research Center, Baltimore, Maryland, USA
    J Neurochem 118:611-5. 2011
    ..Taken together, these observations support the existence of a potentially pathogenic relationship between dietary fat intake, peripheral cholesterol and triglyceride levels, brain cell sphingolipid metabolism, and oxidative stress...
  23. pmc Extension of lifespan in C. elegans by naphthoquinones that act through stress hormesis mechanisms
    Piper R Hunt
    Laboratory of Neurosciences, National Institute on Aging, Intramural Research Program, National Institutes of Health, Baltimore, Maryland, United States of America
    PLoS ONE 6:e21922. 2011
    ..Our findings reveal the potential for low doses of naturally occurring naphthoquinones to extend lifespan by engaging a specific adaptive cellular stress response pathway...
  24. ncbi request reprint Dietary folate deficiency and elevated homocysteine levels endanger dopaminergic neurons in models of Parkinson's disease
    Wenzhen Duan
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, Baltimore, Maryland 21224, USA
    J Neurochem 80:101-10. 2002
    ..The ability of folate deficiency and elevated homocysteine levels to sensitize dopaminergic neurons to environmental toxins suggests a mechanism whereby dietary folate may influence risk for PD...
  25. pmc Chronic mild sleep restriction accentuates contextual memory impairments, and accumulations of cortical Aβ and pTau in a mouse model of Alzheimer's disease
    Sarah M Rothman
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, National Institutes of Health, 251 Bayview Blvd Baltimore, MD 21224, USA
    Brain Res 1529:200-8. 2013
    ....
  26. ncbi request reprint Evidence for miR-181 involvement in neuroinflammatory responses of astrocytes
    Emmette R Hutchison
    Laboratory of Neurosciences, National Institute on Aging, NIH, Baltimore, Maryland, 21224, USA
    Glia 61:1018-28. 2013
    ..Further understanding of the role of miR-181 in inflammatory events and CNS injury could lead to novel approaches for the treatment of CNS disorders with an inflammatory component...
  27. pmc Transferrin fusion technology: a novel approach to prolonging biological half-life of insulinotropic peptides
    Byung Joon Kim
    National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224, USA
    J Pharmacol Exp Ther 334:682-92. 2010
    ..EX-4-Tf proved to be as effective as EX-4 but had longer lived effects on blood glucose and food intake. This novel transferrin fusion technology could improve the pharmacology of various peptides...
  28. pmc Dietary restriction mitigates cocaine-induced alterations of olfactory bulb cellular plasticity and gene expression, and behavior
    Xiangru Xu
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, Maryland, USA
    J Neurochem 114:323-34. 2010
    ..The data further suggest that modification of dietary energy intake could provide a novel potential approach to addiction treatments...
  29. ncbi request reprint Glucagon-like peptide 1 modulates calcium responses to glutamate and membrane depolarization in hippocampal neurons
    Charles P Gilman
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    J Neurochem 87:1137-44. 2003
    ..Collectively, our findings suggest that, by modulating calcium responses to glutamate and membrane depolarization, GLP-1 may play important roles in regulating neuronal plasticity and cell survival...
  30. ncbi request reprint Mitochondrial UCP4 mediates an adaptive shift in energy metabolism and increases the resistance of neurons to metabolic and oxidative stress
    Dong Liu
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD, USA
    Neuromolecular Med 8:389-414. 2006
    ..By shifting energy metabolism to reduce ROS production and cellular reliance on mitochondrial respiration, UCP4 can protect neurons against oxidative stress and calcium overload...
  31. ncbi request reprint Involvement of Gadd153 in the pathogenic action of presenilin-1 mutations
    Ollivier Milhavet
    Laboratory of Neurosciences, National Institute on Aging, Gerontology Research Center, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    J Neurochem 83:673-81. 2002
    ..An abnormality in the translational regulation of Gadd153 may sensitize cells to the detrimental effects of ER stress and contribute to the pathogenic actions of PS1 mutations in FAD...
  32. ncbi request reprint Disruption of neurogenesis by amyloid beta-peptide, and perturbed neural progenitor cell homeostasis, in models of Alzheimer's disease
    Norman J Haughey
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, Baltimore, Maryland 21224, USA
    J Neurochem 83:1509-24. 2002
    ..Adverse effects of Abeta on NPC may contribute to the depletion of neurons and cognitive impairment in AD...
  33. ncbi request reprint Alzheimer's amyloid beta-peptide enhances ATP/gap junction-mediated calcium-wave propagation in astrocytes
    Norman J Haughey
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Neuromolecular Med 3:173-80. 2003
    ..These findings reveal a novel action of Abeta on the propagation of intercellular calcium signals in astrocytes, and also suggests a role for altered astrocyte calcium-signaling in the pathogenesis of AD...
  34. pmc Permeability transition pore-mediated mitochondrial superoxide flashes regulate cortical neural progenitor differentiation
    Yan Hou
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, Maryland, United States of America
    PLoS ONE 8:e76721. 2013
    ..Conversely, manipulations that increase superoxide flash frequency accelerate neuronal differentiation. Our findings reveal a regulatory role for mitochondrial superoxide flashes, mediated by mPTP opening, in neuronal differentiation. ..
  35. ncbi request reprint Evidence that BDNF regulates heart rate by a mechanism involving increased brainstem parasympathetic neuron excitability
    Ruiqian Wan
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, Maryland, USA
    J Neurochem 129:573-80. 2014
    ..Our findings reveal a previously unknown role for BDNF in the control of heart rate by a mechanism involving increased activation of brainstem cholinergic parasympathetic neurons...
  36. pmc Dietary energy intake modifies brainstem autonomic dysfunction caused by mutant α-synuclein
    Kathleen J Griffioen
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA
    Neurobiol Aging 34:928-35. 2013
    ....
  37. pmc Effects of cerium oxide nanoparticles on the growth of keratinocytes, fibroblasts and vascular endothelial cells in cutaneous wound healing
    Srinivasulu Chigurupati
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA
    Biomaterials 34:2194-201. 2013
    ..The Nanoceria penetrated into the wound tissue and reduced oxidative damage to cellular membranes and proteins, suggesting a therapeutic potential for topical treatment of wounds with antioxidant nanoparticles...
  38. doi request reprint 3,6'-dithiothalidomide improves experimental stroke outcome by suppressing neuroinflammation
    Jeong Seon Yoon
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, Maryland 21224, USA
    J Neurosci Res 91:671-80. 2013
    ..These findings suggest that anti-inflammatory mechanisms underlie the therapeutic actions of 3,6-DT in an animal model of stroke...
  39. pmc The KATP channel activator diazoxide ameliorates amyloid-β and tau pathologies and improves memory in the 3xTgAD mouse model of Alzheimer's disease
    Dong Liu
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA
    J Alzheimers Dis 22:443-57. 2010
    ..Our findings show that diazoxide can ameliorate molecular, cytopathological, and behavioral alterations in a mouse model of AD suggesting a therapeutic potential for drugs that activate KATP channels in the treatment of AD...
  40. pmc Toll-like receptor 3 inhibits memory retention and constrains adult hippocampal neurogenesis
    Eitan Okun
    Laboratory of Neurosciences, Intramural Research Program, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA
    Proc Natl Acad Sci U S A 107:15625-30. 2010
    ..Our findings reveal previously undescribed roles for TLR3 as a suppressor of hippocampal cellular plasticity and memory retention...
  41. ncbi request reprint Folic acid deficiency and homocysteine impair DNA repair in hippocampal neurons and sensitize them to amyloid toxicity in experimental models of Alzheimer's disease
    Inna I Kruman
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, Baltimore, Maryland 21224, USA
    J Neurosci 22:1752-62. 2002
    ..Levels of Abeta were unchanged in the brains of folate-deficient APP mutant mice. Our data suggest that folic acid deficiency and homocysteine impair DNA repair in neurons, which sensitizes them to oxidative damage induced by Abeta...
  42. ncbi request reprint Presenilin-1 mutation sensitizes oligodendrocytes to glutamate and amyloid toxicities, and exacerbates white matter damage and memory impairment in mice
    Kirk Pak
    Laboratory of Neurosciences, National Institute of Aging Gerontology Reseasrch Center, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Neuromolecular Med 3:53-64. 2003
    ..These findings demonstrate an adverse effect of a disease-causing PS1 mutation in oligodendrocytes, and suggest a mechanism responsible for white matter damage in AD and a contribution of such damage to cognitive impairment...
  43. pmc Dietary restriction normalizes glucose metabolism and BDNF levels, slows disease progression, and increases survival in huntingtin mutant mice
    Wenzhen Duan
    Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Proc Natl Acad Sci U S A 100:2911-6. 2003
    ..Our findings suggest a dietary intervention that may suppress the disease process and increase the life span of humans that carry the mutant huntingtin gene...
  44. ncbi request reprint Intermittent fasting and caloric restriction ameliorate age-related behavioral deficits in the triple-transgenic mouse model of Alzheimer's disease
    Veerendra Kumar Madala Halagappa
    Laboratory of Neurosciences, National Institute on Aging, Intramural Research Program, Baltimore, MD 21224, USA
    Neurobiol Dis 26:212-20. 2007
    ..We conclude that CR and IF dietary regimens can ameliorate age-related deficits in cognitive function by mechanisms that may or may not be related to Abeta and tau pathologies...
  45. pmc Nicotinamide forestalls pathology and cognitive decline in Alzheimer mice: evidence for improved neuronal bioenergetics and autophagy procession
    Dong Liu
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD, USA
    Neurobiol Aging 34:1564-80. 2013
    ..Thus, nicotinamide suppresses AD pathology and cognitive decline in a mouse model of AD by a mechanism involving improved brain bioenergetics with preserved functionality of mitochondria and the autophagy system...
  46. pmc Neuronal calcium homeostasis and dysregulation
    Marc Gleichmann
    Laboratory of Neurosciences, National Institute on Aging, Baltimore, Maryland, USA
    Antioxid Redox Signal 14:1261-73. 2011
    ....
  47. pmc The excitatory neurotransmitter glutamate stimulates DNA repair to increase neuronal resiliency
    Jenq Lin Yang
    Laboratory of Molecular Gerontology, National Institute on Aging Intramural Research Program, Baltimore, MD, USA
    Mech Ageing Dev 132:405-11. 2011
    ..We conclude that glutamate signaling involves an adaptive cellular stress response pathway that enhances DNA repair capability, thereby protecting neurons against injury and disease...
  48. pmc Neurons efficiently repair glutamate-induced oxidative DNA damage by a process involving CREB-mediated up-regulation of apurinic endonuclease 1
    Jenq Lin Yang
    Laboratory of Molecular Gerontology, National Institute on Aging Intramural Research Program, Baltimore, Maryland 21224, USA
    J Biol Chem 285:28191-9. 2010
    ..Our findings reveal a previously unknown ability of neurons to efficiently repair oxidative DNA lesions after transient activation of glutamate receptors...
  49. pmc Age and energy intake interact to modify cell stress pathways and stroke outcome
    Thiruma V Arumugam
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA
    Ann Neurol 67:41-52. 2010
    ..We therefore determined the interactions of age and energy intake on the outcome of ischemic brain injury, and elucidated the underlying mechanisms...
  50. ncbi request reprint Reversal of behavioral and metabolic abnormalities, and insulin resistance syndrome, by dietary restriction in mice deficient in brain-derived neurotrophic factor
    Wenzhen Duan
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, Baltimore, Maryland 21224, USA
    Endocrinology 144:2446-53. 2003
    ..Dietary and pharmacological manipulations of BDNF signaling may prove useful in the prevention and treatment of obesity and insulin resistance syndrome-related diseases...
  51. ncbi request reprint Numb isoforms containing a short PTB domain promote neurotrophic factor-induced differentiation and neurotrophic factor withdrawal-induced death of PC12 Cells
    Ward A Pedersen
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, Baltimore, Maryland 21224, USA
    J Neurochem 82:976-86. 2002
    ..Our results suggest that Numb sensitizes cells to neurotrophin responses in an isoform-specific manner, an effect that may play an important role in the development and plasticity of the nervous system...
  52. pmc Prophylactic treatment with paroxetine ameliorates behavioral deficits and retards the development of amyloid and tau pathologies in 3xTgAD mice
    Rhonda L Nelson
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD, USA
    Exp Neurol 205:166-76. 2007
    ....
  53. ncbi request reprint Bone marrow transplantation reveals roles for brain macrophage/microglia TNF signaling and nitric oxide production in excitotoxic neuronal death
    Zhihong Guo
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Neuromolecular Med 5:219-34. 2004
    ....
  54. ncbi request reprint Evidence that caspase-1 is a negative regulator of AMPA receptor-mediated long-term potentiation at hippocampal synapses
    Chengbiao Lu
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, Maryland, USA
    J Neurochem 97:1104-10. 2006
    ..These findings suggest that, by selectively reducing AMPA currents and calcium influx, caspase-1 functions as a negative regulator of LTP at hippocampal synapses...
  55. ncbi request reprint Nitric oxide acts in a positive feedback loop with BDNF to regulate neural progenitor cell proliferation and differentiation in the mammalian brain
    Aiwu Cheng
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Dev Biol 258:319-33. 2003
    ....
  56. ncbi request reprint Involvement of superoxide in pathogenic action of mutations that cause Alzheimer's disease
    Mark P Mattson
    Laboratory of Neurosciences, Gerontology Research Center, National Institute on Aging, Baltimore, Maryland 21224, USA
    Methods Enzymol 352:455-74. 2002
  57. ncbi request reprint Involvement of mitochondrial K+ release and cellular efflux in ischemic and apoptotic neuronal death
    Dong Liu
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, Baltimore, Maryland, USA
    J Neurochem 86:966-79. 2003
    ....
  58. ncbi request reprint Dietary restriction enhances neurotrophin expression and neurogenesis in the hippocampus of adult mice
    Jaewon Lee
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center Baltimore, Maryland 21224, USA
    J Neurochem 80:539-47. 2002
    ..The ability of a change in diet to stimulate neurotrophin expression and enhance neurogenesis has important implications for dietary modification of neuroplasticity and responses of the brain to injury and disease...
  59. ncbi request reprint Homocysteine and folate deficiency sensitize oligodendrocytes to the cell death-promoting effects of a presenilin-1 mutation and amyloid beta-peptide
    Kirk J Pak
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Neuromolecular Med 3:119-28. 2003
    ..These findings demonstrate an adverse effect of homocysteine on oligodendrocytes, and suggest roles for homocysteine and folate deficiency in the white matter damage in AD and related neurodegenerative disorders...
  60. pmc Bidirectional metabolic regulation of neurocognitive function
    Alexis M Stranahan
    Department of Psychological and Brain Sciences, Johns Hopkins University, Baltimore, MD 21218, USA
    Neurobiol Learn Mem 96:507-16. 2011
    ..Understanding the mechanisms for this continuum may yield novel therapeutic targets for the prevention and treatment of cognitive decline following aging, disease, or injury...
  61. pmc Endonuclease VIII-like 1 (NEIL1) promotes short-term spatial memory retention and protects from ischemic stroke-induced brain dysfunction and death in mice
    Chandrika Canugovi
    Laboratory of Molecular Gerontology, Intramural Research Program, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA
    Proc Natl Acad Sci U S A 109:14948-53. 2012
    ..These results indicate that NEIL1 plays an important role in learning and memory and in protection of neurons against ischemic injury...
  62. pmc miR-375 inhibits differentiation of neurites by lowering HuD levels
    Kotb Abdelmohsen
    Laboratory of Cellular and Molecular Biology, National Institute on Aging Intramural Research Program, NIH, Baltimore, MD 21224, USA
    Mol Cell Biol 30:4197-210. 2010
    ..Our findings indicate that miR-375 modulates neuronal HuD expression and function, in turn affecting dendrite abundance...
  63. ncbi request reprint Pivotal role for beta-1 integrin in neurovascular remodelling after ischemic stroke
    Justin D Lathia
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA
    Exp Neurol 221:107-14. 2010
    ....
  64. pmc Plumbagin promotes the generation of astrocytes from rat spinal cord neural progenitors via activation of the transcription factor Stat3
    Yongquan Luo
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, Maryland 21224, USA
    J Neurochem 115:1337-49. 2010
    ..These findings demonstrate the ability of a low molecular weight naturally occurring phytochemical to control the fate of glial progenitor cells by a mechanism involving the Stat3 signaling pathway...
  65. pmc Electroconvulsive shock ameliorates disease processes and extends survival in huntingtin mutant mice
    Mohamed R Mughal
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Biomedical Research Center, Baltimore, MD 21224, USA
    Hum Mol Genet 20:659-69. 2011
    ..The potential of ECS as an intervention in subjects that inherit the mutant Htt gene merits further consideration...
  66. pmc Lowering corticosterone levels reinstates hippocampal brain-derived neurotropic factor and Trkb expression without influencing deficits in hypothalamic brain-derived neurotropic factor expression in leptin receptor-deficient mice
    Alexis M Stranahan
    Department of Psychological and Brain Sciences, Johns Hopkins University, Baltimore, MD 21218, USA
    Neuroendocrinology 93:58-64. 2011
    ....
  67. pmc A synthetic uric acid analog accelerates cutaneous wound healing in mice
    Srinivasulu Chigurupati
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, Maryland, United States of America
    PLoS ONE 5:e10044. 2010
    ....
  68. ncbi request reprint Contributions of mitochondrial alterations, resulting from bad genes and a hostile environment, to the pathogenesis of Alzheimer's disease
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Int Rev Neurobiol 53:387-409. 2002
  69. pmc GLP-1 receptor stimulation preserves primary cortical and dopaminergic neurons in cellular and rodent models of stroke and Parkinsonism
    Yazhou Li
    Laboratory of Neurosciences, Intramural Research Program, National Institute on Aging, Baltimore, MD 21224, USA
    Proc Natl Acad Sci U S A 106:1285-90. 2009
    ..Our findings demonstrate that Ex-4 can protect neurons against metabolic and oxidative insults, and they provide preclinical support for the therapeutic potential for Ex-4 in the treatment of stroke and PD...
  70. ncbi request reprint Adult glial precursor proliferation in mutant SOD1G93A mice
    Tim Magnus
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, National Institutes of Health, Baltimore, Maryland 21287, USA
    Glia 56:200-8. 2008
    ..These data suggest that adult glial progenitors from SOD1G93A mice differentially respond to inflammatory cytokines and contribute to the observed reactive astrocytosis observed in SOD1G93A mouse lumbar spinal cord...
  71. ncbi request reprint Leptin-mediated cell survival signaling in hippocampal neurons mediated by JAK STAT3 and mitochondrial stabilization
    Zhihong Guo
    Laboratory of Neurosciences and National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA
    J Biol Chem 283:1754-63. 2008
    ..By enhancing mitochondrial resistance to apoptosis and excitotoxicity, our findings suggest that leptin signaling serves a neurotrophic function in the developing and adult hippocampus...
  72. ncbi request reprint Interactive effects of excitotoxic injury and dietary restriction on microgliosis and neurogenesis in the hippocampus of adult mice
    Jaewon Lee
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Neuromolecular Med 4:179-96. 2003
    ..Our findings show that DR suppresses injuryinduced microgliosis suggesting a contribution of a reduced microglial response to the neuroprotective effects of DR...
  73. ncbi request reprint Phenformin suppresses calcium responses to glutamate and protects hippocampal neurons against excitotoxicity
    Jaewon Lee
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, 5600 Nathan Shock Drive, Baltimore, Maryland 21224, USA
    Exp Neurol 175:161-7. 2002
    ..These findings show that phenformin can modulate neuronal responses to glutamate, and suggest possible use of phenformin and related compounds in the prevention and/or treatment of neurodegenerative conditions...
  74. ncbi request reprint Evidence that brain-derived neurotrophic factor is required for basal neurogenesis and mediates, in part, the enhancement of neurogenesis by dietary restriction in the hippocampus of adult mice
    Jaewon Lee
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, Baltimore, Maryland 21224, USA
    J Neurochem 82:1367-75. 2002
    ....
  75. ncbi request reprint Evidence that accumulation of ceramides and cholesterol esters mediates oxidative stress-induced death of motor neurons in amyotrophic lateral sclerosis
    Roy G Cutler
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, Baltimore, MD, USA
    Ann Neurol 52:448-57. 2002
    ..These findings suggest a pivotal role for altered sphingolipid metabolism in the pathogenesis of ALS...
  76. pmc L-type Ca2+ currents at CA1 synapses, but not CA3 or dentate granule neuron synapses, are increased in 3xTgAD mice in an age-dependent manner
    Yue Wang
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD, USA Electronic address
    Neurobiol Aging 35:88-95. 2014
    ..These findings suggest a potential contribution of altered L-VGCC to the selective vulnerability of CA1 neurons to tau pathology in the 3xTgAD mice and to their degeneration in AD patients. ..
  77. pmc Aberrant heart rate and brainstem brain-derived neurotrophic factor (BDNF) signaling in a mouse model of Huntington's disease
    Kathleen J Griffioen
    Laboratory of Neurosciences, National Institute on Aging, Intramural Research Program, National Institutes of Health, Baltimore, MD, USA
    Neurobiol Aging 33:1481.e1-5. 2012
    ..Our findings establish a link between diminished BDNF expression in brainstem cardiovascular nuclei and abnormal heart rates in HD mice, and suggest a novel therapeutic target for correcting cardiovascular dysfunction in HD...
  78. pmc Stromal factors SDF1α, sFRP1, and VEGFD induce dopaminergic neuron differentiation of human pluripotent stem cells
    Catherine M Schwartz
    National Institute on Aging Intramural Research Program, National Institutes of Health, Laboratory of Neurosciences, Baltimore, MD 21224, USA
    J Neurosci Res 90:1367-81. 2012
    ..These results indicate that SDF1α, sFRP1, and VEGFD are major components of SDIA and suggest the potential use of these defined factors to elicit DA differentiation of pluripotent human stem cells for therapeutic intervention in PD...
  79. pmc Nontelomeric splice variant of telomere repeat-binding factor 2 maintains neuronal traits by sequestering repressor element 1-silencing transcription factor
    Peisu Zhang
    Laboratories of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA
    Proc Natl Acad Sci U S A 108:16434-9. 2011
    ..Thus, TRF2-S acts as part of a unique developmentally regulated molecular switch that plays critical roles in the maintenance and plasticity of neurons...
  80. pmc GLP-1 receptor stimulation depresses heart rate variability and inhibits neurotransmission to cardiac vagal neurons
    Kathleen J Griffioen
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, National Institutes of Health, 251 Bayview Boulevard, Baltimore, MD 21224, USA
    Cardiovasc Res 89:72-8. 2011
    ..We used the long-lasting GLP-1 receptor agonist Exendin-4 (Ex-4) to test the hypothesis that GLP-1 signalling modulates central parasympathetic control of heart rate...
  81. pmc Activity-induced Notch signaling in neurons requires Arc/Arg3.1 and is essential for synaptic plasticity in hippocampal networks
    Lavinia Alberi
    Institute for Cell Engineering, Neuroregeneration Program, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Neuron 69:437-44. 2011
    ..Thus, Notch signaling is dynamically regulated in response to neuronal activity, Arc/Arg3.1 is a context-dependent Notch regulator, and Notch1 is required for the synaptic plasticity that contributes to memory formation...
  82. pmc Cardioprotective effect of intermittent fasting is associated with an elevation of adiponectin levels in rats
    Ruiqian Wan
    Laboratory of Neurosciences, National Institute on Aging, Intramural Research Program, National Institutes of Health, Baltimore, MD, USA
    J Nutr Biochem 21:413-7. 2010
    ..Because recent studies have shown that adiponectin can protect the heart against ischemic injury, our findings suggest a potential role for adiponectin as a mediator of the cardioprotective effect of IF...
  83. pmc Monoamine oxidases regulate telencephalic neural progenitors in late embryonic and early postnatal development
    Aiwu Cheng
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, Maryland 21224, USA
    J Neurosci 30:10752-62. 2010
    ..Our findings reveal novel roles for MAOs and serotonin in the regulation of IPC proliferation in the developing brain...
  84. pmc Clathrin assembly proteins AP180 and CALM in the embryonic rat brain
    Catherine M Schwartz
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, Maryland 21224, USA
    J Comp Neurol 518:3803-18. 2010
    ..These results identify the developmental stage of AP180 and CALM expression and suggest that each protein has distinct functions in neural development...
  85. pmc Preventing NAD(+) depletion protects neurons against excitotoxicity: bioenergetic effects of mild mitochondrial uncoupling and caloric restriction
    Dong Liu
    Laboratory of Neurosciences, Intramural Research Program, National Institute on Aging, Baltimore, MD 21224, USA
    Ann N Y Acad Sci 1147:275-82. 2008
    ..Our findings suggest that mild mitochondrial uncoupling and caloric restriction exert hormetic effects by stimulating bioenergetics in neurons thereby increasing tolerance of neurons to metabolic stress...
  86. pmc Evidence that gamma-secretase mediates oxidative stress-induced beta-secretase expression in Alzheimer's disease
    Dong Gyu Jo
    Laboratory of Neurosciences, National Institute on Aging, Intramural Research Program, Baltimore, MD 21224, USA
    Neurobiol Aging 31:917-25. 2010
    ..Our findings suggest that gamma-secretase mediates oxidative stress-induced expression of BACE1 resulting in excessive Abeta production in AD...
  87. ncbi request reprint Patterns of laminins and integrins in the embryonic ventricular zone of the CNS
    Justin D Lathia
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, 5600 Nathan Shock Drive, Baltimore, Maryland 21224, USA
    J Comp Neurol 505:630-43. 2007
    ....
  88. ncbi request reprint Impaired SDF1/CXCR4 signaling in glial progenitors derived from SOD1(G93A) mice
    Yongquan Luo
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, Maryland, USA
    J Neurosci Res 85:2422-32. 2007
    ..These data indicate that the abnormalities in SOD1(G93A) glial progenitor expression of CXCR4 and its mediated signaling and function occur during spinal cord development and highlight nonneuronal (glial) abnormalities in this ALS model...
  89. ncbi request reprint Pancortin-2 interacts with WAVE1 and Bcl-xL in a mitochondria-associated protein complex that mediates ischemic neuronal death
    Aiwu Cheng
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, Maryland 21224, USA
    J Neurosci 27:1519-28. 2007
    ..Thus, pancortin-2 is a mediator of ischemia-induced apoptosis of neurons in the adult cerebral cortex and functions in a novel mitochondrial/actin-associated protein complex that sequesters Bcl-xL...
  90. pmc Caloric restriction increases neurotrophic factor levels and attenuates neurochemical and behavioral deficits in a primate model of Parkinson's disease
    Navin Maswood
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Proc Natl Acad Sci U S A 101:18171-6. 2004
    ....
  91. ncbi request reprint Phosphatidylinositol-3-kinase-Akt kinase and p42/p44 mitogen-activated protein kinases mediate neurotrophic and excitoprotective actions of a secreted form of amyloid precursor protein
    Guanjun Cheng
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, 5600 Nathan Shock Drive, Baltimore, Maryland 21224, USA
    Exp Neurol 175:407-14. 2002
    ....
  92. ncbi request reprint Urocortin, but not urocortin II, protects cultured hippocampal neurons from oxidative and excitotoxic cell death via corticotropin-releasing hormone receptor type I
    Ward A Pedersen
    Laboratory of Neurosciences, Gerontology Research Center, National Institute on Aging, Baltimore, Maryland 21224, USA
    J Neurosci 22:404-12. 2002
    ..This is the first demonstration of a biological activity of urocortin in hippocampal neurons, suggesting a role for the peptide in adaptive responses of hippocampal neurons to potentially lethal oxidative and excitotoxic insults...
  93. pmc Involvement of oxidative stress-induced abnormalities in ceramide and cholesterol metabolism in brain aging and Alzheimer's disease
    Roy G Cutler
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Proc Natl Acad Sci U S A 101:2070-5. 2004
    ....
  94. ncbi request reprint p53 is present in synapses where it mediates mitochondrial dysfunction and synaptic degeneration in response to DNA damage, and oxidative and excitotoxic insults
    Charles P Gilman
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA
    Neuromolecular Med 3:159-72. 2003
    ....
  95. ncbi request reprint Activation of mitochondrial ATP-dependent potassium channels protects neurons against ischemia-induced death by a mechanism involving suppression of Bax translocation and cytochrome c release
    Dong Liu
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, Baltimore, Maryland 21224, USA
    J Cereb Blood Flow Metab 22:431-43. 2002
    ....
  96. pmc Tumor necrosis factor-alpha-induced neutral sphingomyelinase-2 modulates synaptic plasticity by controlling the membrane insertion of NMDA receptors
    David Wheeler
    Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    J Neurochem 109:1237-49. 2009
    ....
  97. doi request reprint Homeostatic disinhibition in the aging brain and Alzheimer's disease
    Marc Gleichmann
    Laboratory of Neurosciences, National Institute on Aging, Baltimore, MD, USA
    J Alzheimers Dis 24:15-24. 2011
    ..Alternatively, further reduction of GABAergic signaling may work as well, although care has to be taken to prevent epileptic seizures...
  98. pmc The therapeutic potential of microRNAs in nervous system damage, degeneration, and repair
    Emmette R Hutchison
    Laboratory of Neurosciences, National Institute on Aging, Intramural Research Program, Baltimore, MD 21224, USA
    Neuromolecular Med 11:153-61. 2009
    ..Finally, miRNAs have been shown to control cellular proliferation and specification, suggesting that manipulation of miRNAs in cultured cells could result in more convenient generation of pure cell populations for transplantation...
  99. pmc Caloric restriction: impact upon pituitary function and reproduction
    Bronwen Martin
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Ageing Res Rev 7:209-24. 2008
    ....
  100. pmc Mitochondria and neuroplasticity
    Aiwu Cheng
    Laboratory of Neurosciences, National Institute of Aging Intramural Research Program, Baltimore, MD 21224, U S A
    ASN Neuro 2:e00045. 2010
    ..Disturbances in mitochondrial functions and signalling may play roles in impaired neuroplasticity and neuronal degeneration in Alzheimer's disease, Parkinson's disease, psychiatric disorders and stroke...
  101. pmc Diminished iron concentrations increase adenosine A(2A) receptor levels in mouse striatum and cultured human neuroblastoma cells
    Seema Gulyani
    Neurology Department, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    Exp Neurol 215:236-42. 2009
    ..In conclusion, the A(2A)R is increased across different iron-insufficient conditions. The relation between A(2A)R and cellular iron status may be an important pathway by which adenosine may alter the function of the dopaminergic system...