Mark P Mattson

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. doi request reprint Excitation BolsTORs motor neurons in ALS mice
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA Electronic address
    Neuron 80:1-3. 2013
  2. 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
  3. 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
  4. 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
  5. ncbi request reprint Evidence that nucleocytoplasmic Olig2 translocation mediates brain-injury-induced differentiation of glial precursors to astrocytes
    Tim Magnus
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, National Institutes of Health, Baltimore, Maryland 21224, USA
    J Neurosci Res 85:2126-37. 2007
  6. 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
  7. 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
  8. 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
  9. ncbi request reprint Herp stabilizes neuronal Ca2+ homeostasis and mitochondrial function during endoplasmic reticulum stress
    Sic L Chan
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Gerontology Research Center, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    J Biol Chem 279:28733-43. 2004
  10. 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

Collaborators

Detail Information

Publications64

  1. doi request reprint Excitation BolsTORs motor neurons in ALS mice
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA Electronic address
    Neuron 80:1-3. 2013
    ..Saxena et al. (2013) demonstrate that excitation of motor neurons can prevent their demise in a mouse model of inherited ALS by a mechanism involving the mTOR pathway. ..
  2. 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
    ....
  3. 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...
  4. 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...
  5. ncbi request reprint Evidence that nucleocytoplasmic Olig2 translocation mediates brain-injury-induced differentiation of glial precursors to astrocytes
    Tim Magnus
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, National Institutes of Health, Baltimore, Maryland 21224, USA
    J Neurosci Res 85:2126-37. 2007
    ..In contrast, neural stem cells and neuronal progenitor cells appear to play only a minor role in the injured adult CNS...
  6. 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...
  7. 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...
  8. 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...
  9. ncbi request reprint Herp stabilizes neuronal Ca2+ homeostasis and mitochondrial function during endoplasmic reticulum stress
    Sic L Chan
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Gerontology Research Center, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    J Biol Chem 279:28733-43. 2004
    ..By stabilizing ER Ca(2+) homeostasis and mitochondrial functions, Herp serves a neuroprotective function under conditions of ER stress...
  10. 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
    ....
  11. 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...
  12. 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
    ....
  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 Impaired long-term depression in P2X3 deficient mice is not associated with a spatial learning deficit
    Yue Wang
    Laboratory of Neurosciences, National Institute on Aging, Baltimore, MD 21224, USA
    J Neurochem 99:1425-34. 2006
    ....
  15. 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...
  16. 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
    ....
  17. pmc Presenilin-1 mutation impairs cholinergic modulation of synaptic plasticity and suppresses NMDA currents in hippocampus slices
    Yue Wang
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Gerontology Research Center, Baltimore, MD 21224, USA
    Neurobiol Aging 30:1061-8. 2009
    ....
  18. doi 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
    ....
  19. 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...
  20. 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...
  21. pmc Toll-like receptor-4 mediates neuronal apoptosis induced by amyloid beta-peptide and the membrane lipid peroxidation product 4-hydroxynonenal
    Sung Chun Tang
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA
    Exp Neurol 213:114-21. 2008
    ..Our findings suggest that TLR4 signaling increases the vulnerability of neurons to Abeta and oxidative stress in AD, and identify TLR4 as a potential therapeutic target for AD...
  22. 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...
  23. 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...
  24. 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
    ....
  25. 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...
  26. 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...
  27. pmc Toll-like receptor 3 is a negative regulator of embryonic neural progenitor cell proliferation
    Justin D Lathia
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, Maryland 21224, USA
    J Neurosci 28:13978-84. 2008
    ..Our findings reveal a novel role for TLR3 in the negative regulation of NPC proliferation in the developing brain...
  28. 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...
  29. ncbi request reprint Suppression of calcium release from inositol 1,4,5-trisphosphate-sensitive stores mediates the anti-apoptotic function of nuclear factor-kappaB
    Simonetta Camandola
    Laboratory of Neurosciences, National Institute on Aging NIH, Gerontology Research Center, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    J Biol Chem 280:22287-96. 2005
    ..Overexpression of Bcl-2 normalizes ER calcium homeostasis and prevents calcium-mediated apoptosis in RelA-deficient cells. These findings establish an ER calcium channel as a pivotal target for NF-kappaB-mediated cell survival signaling...
  30. 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
    ....
  31. 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...
  32. 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...
  33. ncbi request reprint Soluble neuroprotective antioxidant uric acid analogs ameliorate ischemic brain injury in mice
    Frank Haberman
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, 5600 Nathan Shock Drive, Baltimore, MD, USA
    Neuromolecular Med 9:315-23. 2007
    ..These findings suggest a therapeutic potential for soluble analogs of uric acid in the treatment of stroke and related neurodegenerative conditions...
  34. 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...
  35. 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
    ....
  36. 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
    ....
  37. 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...
  38. pmc Intravenous immunoglobulin (IVIG) protects the brain against experimental stroke by preventing complement-mediated neuronal cell death
    Thiruma V Arumugam
    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 104:14104-9. 2007
    ..Our data suggest a major role for complement-mediated cell death in ischemic brain injury and the prospect of using IVIG in relatively low doses as an interventional therapy for stroke...
  39. 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...
  40. 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...
  41. ncbi request reprint Truncated tyrosine kinase B brain-derived neurotrophic factor receptor directs cortical neural stem cells to a glial cell fate by a novel signaling mechanism
    Aiwu Cheng
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, Maryland 21224, USA
    J Neurochem 100:1515-30. 2007
    ..Our findings suggest a mechanism by which a single factor (BDNF) regulates the production of the two major cell types in the mammalian cerebral cortex...
  42. 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...
  43. 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...
  44. 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...
  45. 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...
  46. 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...
  47. 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...
  48. ncbi request reprint Gap junctional communication is required to maintain mouse cortical neural progenitor cells in a proliferative state
    Aiwu Cheng
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA
    Dev Biol 272:203-16. 2004
    ..In addition to promoting their proliferation, gap junctions are required for the survival of NPCs. Gap junctional communication is therefore both necessary and sufficient to maintain NPCs in a self-renewing state...
  49. ncbi request reprint Telomere protection mechanisms change during neurogenesis and neuronal maturation: newly generated neurons are hypersensitive to telomere and DNA damage
    Aiwu Cheng
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, Maryland 21224, USA
    J Neurosci 27:3722-33. 2007
    ....
  50. 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...
  51. 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...
  52. 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
    ....
  53. pmc Pivotal role for neuronal Toll-like receptors in ischemic brain injury and functional deficits
    Sung Chun Tang
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA
    Proc Natl Acad Sci U S A 104:13798-803. 2007
    ..Our findings establish a proapoptotic signaling pathway for TLR2 and -4 in neurons that may render them vulnerable to ischemic death...
  54. ncbi request reprint Neuroprotective actions of a histidine analogue in models of ischemic stroke
    Sung Chun Tang
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, Maryland 21224, USA
    J Neurochem 101:729-36. 2007
    ..These findings suggest a therapeutic potential for HNE-scavenging histidine analogues in the treatment of stroke and related neurodegenerative conditions...
  55. pmc Lifelong running reduces oxidative stress and degenerative changes in the testes of mice
    Srinivasulu Chigurupati
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, Maryland 21224, USA
    J Endocrinol 199:333-41. 2008
    ..These findings suggest that lifelong regular exercise suppresses aging of testes by a mechanism that involves reduced oxidative damage to spermatogenic and Leydig cells...
  56. pmc DNA base excision repair activities in mouse models of Alzheimer's disease
    Lior Weissman
    Laboratory of Molecular Gerontology, National Institute on Aging, NIH, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Neurobiol Aging 30:2080-1. 2009
    ..Our results suggest that unlike in humans, the development of AD-like pathology in the studied mouse models is not associated with deficiencies in BER...
  57. 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...
  58. 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...
  59. 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...
  60. 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
    ....
  61. 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...
  62. ncbi request reprint Up-regulation of plasma membrane-associated redox activities in neuronal cells lacking functional mitochondria
    Dong Hoon Hyun
    Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224, USA
    J Neurochem 100:1364-74. 2007
    ....
  63. 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...
  64. 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...