M P Mattson

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. ncbi Transcriptome coexpression map of human embryonic stem cells
    Huai Li
    Bioinformatics Unit, Branch of Research Resources, National Institute on Aging, NIH, Baltimore, MD 21224, USA
    BMC Genomics 7:103. 2006
  2. ncbi Energy intake and exercise as determinants of brain health and vulnerability to injury and disease
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, 251 Bayview Boulevard, Baltimore, MD 21224, USA
    Cell Metab 16:706-22. 2012
  3. ncbi Evolutionary aspects of human exercise--born to run purposefully
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA
    Ageing Res Rev 11:347-52. 2012
  4. ncbi Gene expression atlas of the mouse central nervous system: impact and interactions of age, energy intake and gender
    Xiangru Xu
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Genome Biol 8:R234. 2007
  5. ncbi Evidence that adiponectin receptor 1 activation exacerbates ischemic neuronal death
    John Thundyil
    School of Biomedical Sciences, University of Queensland, Brisbane, Queensland 4072, Australia
    Exp Transl Stroke Med 2:15. 2010
  6. ncbi 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
  7. ncbi Cell-extracellular matrix interactions regulate neural differentiation of human embryonic stem cells
    Wu Ma
    Stem Cell Center, Developmental Biology, American Type Culture Collection, Manassas, VA, USA
    BMC Dev Biol 8:90. 2008
  8. ncbi Genome wide profiling of human embryonic stem cells (hESCs), their derivatives and embryonal carcinoma cells to develop base profiles of U.S. Federal government approved hESC lines
    Ying Liu
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, National Institutes of Health, Baltimore, Maryland 21224, USA
    BMC Dev Biol 6:20. 2006
  9. ncbi Self-renewal and differentiation capabilities are variable between human embryonic stem cell lines I3, I6 and BG01V
    Tahereh Tavakoli
    Stem Cell Center, Developmental Biology, American Type Culture Collection, Manassas, VA, USA
    BMC Cell Biol 10:44. 2009
  10. ncbi Metal-catalyzed disruption of membrane protein and lipid signaling in the pathogenesis of neurodegenerative disorders
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, and Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21224, USA
    Ann N Y Acad Sci 1012:37-50. 2004

Collaborators

Detail Information

Publications202 found, 100 shown here

  1. ncbi Transcriptome coexpression map of human embryonic stem cells
    Huai Li
    Bioinformatics Unit, Branch of Research Resources, National Institute on Aging, NIH, Baltimore, MD 21224, USA
    BMC Genomics 7:103. 2006
    ..However, no systematic analysis has yet addressed whether gene expression in human ES cells may be regulated in chromosomal domains, and no chromosomal domains of coexpression have been identified...
  2. ncbi Energy intake and exercise as determinants of brain health and vulnerability to injury and disease
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, 251 Bayview Boulevard, Baltimore, MD 21224, USA
    Cell Metab 16:706-22. 2012
    ..Intense concerted efforts of governments, families, schools, and physicians will be required to successfully implement brain-healthy lifestyles that incorporate ER and exercise...
  3. ncbi Evolutionary aspects of human exercise--born to run purposefully
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA
    Ageing Res Rev 11:347-52. 2012
    ..A better understanding of such 'healthspan-extending' actions of endurance exercise may lead to new approaches for improving quality of life as we advance in the coming decades and centuries...
  4. ncbi Gene expression atlas of the mouse central nervous system: impact and interactions of age, energy intake and gender
    Xiangru Xu
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Genome Biol 8:R234. 2007
    ..The structural and functional complexity of the mammalian central nervous system (CNS) is organized and modified by complicated molecular signaling processes that are poorly understood...
  5. ncbi Evidence that adiponectin receptor 1 activation exacerbates ischemic neuronal death
    John Thundyil
    School of Biomedical Sciences, University of Queensland, Brisbane, Queensland 4072, Australia
    Exp Transl Stroke Med 2:15. 2010
    ..We show that cortical neurons express ADRs and reveal a pro-apoptotic role for ADR1 activation in neurons, which may render them vulnerable to ischemic death...
  6. ncbi 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...
  7. ncbi Cell-extracellular matrix interactions regulate neural differentiation of human embryonic stem cells
    Wu Ma
    Stem Cell Center, Developmental Biology, American Type Culture Collection, Manassas, VA, USA
    BMC Dev Biol 8:90. 2008
    ..However, the ECM is a complex mixture of matrix molecules; little is known about the role of ECM components in human embryonic stem cell (hESC) differentiation into neural progenitors and neurons...
  8. ncbi Genome wide profiling of human embryonic stem cells (hESCs), their derivatives and embryonal carcinoma cells to develop base profiles of U.S. Federal government approved hESC lines
    Ying Liu
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, National Institutes of Health, Baltimore, Maryland 21224, USA
    BMC Dev Biol 6:20. 2006
    ....
  9. ncbi Self-renewal and differentiation capabilities are variable between human embryonic stem cell lines I3, I6 and BG01V
    Tahereh Tavakoli
    Stem Cell Center, Developmental Biology, American Type Culture Collection, Manassas, VA, USA
    BMC Cell Biol 10:44. 2009
    ..Lines I3 and I6 possess normal XX and a normal XY karyotype while BG01V is a variant cell line with an abnormal karyotype derived from the karyotypically normal cell line BG01...
  10. ncbi Metal-catalyzed disruption of membrane protein and lipid signaling in the pathogenesis of neurodegenerative disorders
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, and Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21224, USA
    Ann N Y Acad Sci 1012:37-50. 2004
    ..Novel preventative and therapeutic approaches for neurodegenerative disorders are emerging from basic research on the molecular and cellular actions of metals and MAOS in neural cells...
  11. ncbi Infectious agents and age-related neurodegenerative disorders
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging, Gerontology Research Center, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Ageing Res Rev 3:105-20. 2004
    ..In the case of stroke, blood vessels may be adversely affected by bacteria or viruses resulting in atherosclerosis...
  12. ncbi Pathways towards and away from Alzheimer's disease
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, 5600 Nathan Shock Drive, Baltimore, Maryland 21224, USA
    Nature 430:631-9. 2004
    ..But rapid progress towards understanding the cellular and molecular alterations that are responsible for the neuron's demise may soon help in developing effective preventative and therapeutic strategies...
  13. ncbi Folic acid and homocysteine in age-related disease
    Mark P Mattson
    Laboratory of Neurosciences, Gerontology Research Center, National Institute on Aging, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Ageing Res Rev 1:95-111. 2002
    ....
  14. ncbi A neural signaling triumvirate that influences ageing and age-related disease: insulin/IGF-1, BDNF and serotonin
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD, USA
    Ageing Res Rev 3:445-64. 2004
    ....
  15. ncbi Prophylactic activation of neuroprotective stress response pathways by dietary and behavioral manipulations
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, Baltimore, Maryland 21224, USA
    NeuroRx 1:111-6. 2004
    ....
  16. ncbi Beneficial effects of intermittent fasting and caloric restriction on the cardiovascular and cerebrovascular systems
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA
    J Nutr Biochem 16:129-37. 2005
    ..A better understanding of the cellular and molecular mechanisms by which IF and CR affect the blood vessels and heart and brain cells will likely lead to novel preventative and therapeutic strategies for extending health span...
  17. 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...
  18. ncbi Adventures in neural plasticity, aging, and neurodegenerative disorders aboard the CWC beagle
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, 5600 Nathan Shock Drive, Baltimore, Maryland, USA
    Neurochem Res 28:1631-7. 2003
    ....
  19. ncbi Perturbed signal transduction in neurodegenerative disorders involving aberrant protein aggregation
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, Baltimore, MD 21224, USA
    Neuromolecular Med 4:109-32. 2003
    ..A better understanding of how abnormal protein aggregation occurs and how it affects and is affected by specific signal transduction pathways, is leading to novel approaches for preventing and treating neurodegenerative disorders...
  20. ncbi Gene-diet interactions in brain aging and neurodegenerative disorders
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging, Gerontology Research Center 4F01, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Ann Intern Med 139:441-4. 2003
    ....
  21. ncbi Modification of brain aging and neurodegenerative disorders by genes, diet, and behavior
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, Baltimore, Maryland 21224, USA
    Physiol Rev 82:637-72. 2002
    ..The recent application of modern methods of molecular and cellular biology to the problem of brain aging is revealing a remarkable capacity within brain cells for adaptation to aging and resistance to disease...
  22. ncbi Neuroprotective and neurorestorative signal transduction mechanisms in brain aging: modification by genes, diet and behavior
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center 4F01, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Neurobiol Aging 23:695-705. 2002
    ..The recent application of modem methods of molecular and cellular biology to the problem of brain aging is revealing a remarkable capacity within brain cells for adaptation to aging and resistance to disease...
  23. ncbi Energetics and oxidative stress in synaptic plasticity and neurodegenerative disorders
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, Baltimore, MD 21224, USA
    Neuromolecular Med 2:215-31. 2002
    ....
  24. ncbi Will caloric restriction and folate protect against AD and PD?
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging, Gerontology Research Center, Baltimore, MD 21224, USA
    Neurology 60:690-5. 2003
    ..Although further studies are required in humans, the emerging data suggest that high-calorie diets and elevated homocysteine levels may render the brain vulnerable to neurodegenerative disorders...
  25. ncbi Methylation and acetylation in nervous system development and neurodegenerative disorders
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Ageing Res Rev 2:329-42. 2003
    ..Interestingly, dietary factors that influence DNA methylation may affect the risk of neurodegenerative disorders, for example, individuals with low dietary folate intake are at increased risk of Alzheimer's and Parkinson's diseases...
  26. ncbi Excitotoxic and excitoprotective mechanisms: abundant targets for the prevention and treatment of neurodegenerative disorders
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Neuromolecular Med 3:65-94. 2003
    ..A better understanding of the excitotoxic process is not only leading to the development of novel therapeutic approaches for neurodegenerative disorders, but also to unexpected insight into mechanisms of synaptic plasticity...
  27. ncbi Mitochondrial potassium channels and uncoupling proteins in synaptic plasticity and neuronal cell death
    Mark P Mattson
    Laboratory of Neurosciences, Gerontology Research Center, National Institute on Aging, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Biochem Biophys Res Commun 304:539-49. 2003
    ..In addition to their roles in neuronal cell survival and death, MitoKATP channels and UCPs may play roles in regulating neuronal differentiation during development and synaptic plasticity in the adult...
  28. ncbi Mitochondria in cell death: novel targets for neuroprotection and cardioprotection
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Trends Mol Med 9:196-205. 2003
    ..In addition, manipulations that modulate the expression or activity of mitochondrial uncoupling proteins can prevent the death of post-mitotic cells. Such agents hold promise for use in clinical neuroprotection and cardioprotection...
  29. ncbi Folate and homocysteine metabolism: therapeutic targets in cardiovascular and neurodegenerative disorders
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Curr Med Chem 10:1923-9. 2003
    ..Dietary folate stimulates homocysteine removal and may thereby protect cells against disease processes. The enzymes involved in homocysteine and folate metabolism provide novel targets for drug discovery...
  30. ncbi Neuronal and glial calcium signaling in Alzheimer's disease
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging, Gerontology Research Center 4F01, Baltimore, MD 21224, USA
    Cell Calcium 34:385-97. 2003
    ....
  31. ncbi How does the brain control lifespan?
    Mark P Mattson
    Laboratory of Neurosciences 4F02, National Institute on Aging Gerontology Research Center, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Ageing Res Rev 1:155-65. 2002
    ..Roles for other evolutionarily conserved brain signaling pathways in lifespan determination are likely to be discovered in the near future...
  32. ncbi The need for controlled studies of the effects of meal frequency on health
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Lancet 365:1978-80. 2005
  33. ncbi Energy intake, meal frequency, and health: a neurobiological perspective
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, and Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    Annu Rev Nutr 25:237-60. 2005
    ..A better understanding of the neurobiological mechanisms by which meal size and frequency affect human health may lead to novel approaches for disease prevention and treatment...
  34. ncbi Neurotrophic factors in autonomic nervous system plasticity and dysfunction
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD USA
    Neuromolecular Med 10:157-68. 2008
    ....
  35. ncbi Hormesis and disease resistance: activation of cellular stress response pathways
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA
    Hum Exp Toxicol 27:155-62. 2008
    ..Knowledge of hormesis mechanisms is leading to novel approaches for preventing and treating a range of human diseases...
  36. ncbi Awareness of hormesis will enhance future research in basic and applied neuroscience
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, Maryland 21224, USA
    Crit Rev Toxicol 38:633-9. 2008
    ..The development of interventions that activate hormetic signaling pathways in neurons is a promising new approach for the preventation and treatment of a range of neurological disorders...
  37. ncbi No more brain tangles with DeltaNp73
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA
    Trends Biochem Sci 34:6-8. 2009
    ..These findings provide a novel animal model of AD and a potential therapeutic role for DeltaNp73 inducers...
  38. ncbi Glutamate and neurotrophic factors in neuronal plasticity and disease
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA
    Ann N Y Acad Sci 1144:97-112. 2008
    ..By enhancing neurotrophic factor signaling, environmental factors such as exercise and dietary energy restriction, and chemicals such as antidepressants may optimize glutamatergic signaling and protect against neurological disorders...
  39. ncbi Mitochondria in neuroplasticity and neurological disorders
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA
    Neuron 60:748-66. 2008
    ..Advances in understanding the molecular and cell biology of mitochondria are leading to novel approaches for the prevention and treatment of neurological disorders...
  40. ncbi Live longer sans the AT1A receptor
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA
    Cell Metab 9:403-5. 2009
    ..AT(1A)R-deficient mice live longer and have lower levels of oxidative stress than wild-type mice (Benigni et al., 2009), suggesting a role for AT(1A)R signaling in the aging process...
  41. ncbi Roles of the lipid peroxidation product 4-hydroxynonenal in obesity, the metabolic syndrome, and associated vascular and neurodegenerative disorders
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA
    Exp Gerontol 44:625-33. 2009
    ..The recent development of low molecular weight molecules that scavenge HNE suggests that HNE can be targeted in the design of drugs for the treatment of obesity, the metabolic syndrome, and associated disorders...
  42. ncbi Perspective: Does brown fat protect against diseases of aging?
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA
    Ageing Res Rev 9:69-76. 2010
    ....
  43. ncbi ER calcium and Alzheimer's disease: in a state of flux
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA
    Sci Signal 3:pe10. 2010
    ....
  44. ncbi Hormesis defined
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA
    Ageing Res Rev 7:1-7. 2008
    ..A better understanding of hormesis mechanisms at the cellular and molecular levels is leading to and to novel approaches for the prevention and treatment of many different diseases...
  45. ncbi Dietary factors, hormesis and health
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA
    Ageing Res Rev 7:43-8. 2008
    ....
  46. ncbi NF-kappaB in the survival and plasticity of neurons
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Neurochem Res 30:883-93. 2005
    ..NF-kappaB provides an attractive target for the development of novel therapeutic approaches for a range of neurological disorders...
  47. ncbi The neuronal death protein par-4 mediates dopaminergic synaptic plasticity
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA
    Mol Interv 5:278-81. 2005
    ....
  48. 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...
  49. ncbi Ageing and neuronal vulnerability
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, Maryland 21224 6825, USA
    Nat Rev Neurosci 7:278-94. 2006
    ....
  50. ncbi Caloric restriction and intermittent fasting alter spectral measures of heart rate and blood pressure variability in rats
    Donald E Mager
    Laboratory of Neurosciences, National Institute on Aging, 5600 Nathan Shock Dr, Baltimore, MD 21224, USA
    FASEB J 20:631-7. 2006
    ..These results suggest an additional cardiovascular benefit of DR that merits further studies of this potential effect in humans...
  51. ncbi Neurohormetic phytochemicals: Low-dose toxins that induce adaptive neuronal stress responses
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA
    Trends Neurosci 29:632-9. 2006
    ..Thus, as we discuss in this review, highly conserved longevity and survival pathways in neurons are the targets of many phytochemicals...
  52. ncbi Mitochondrial regulation of neuronal plasticity
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Neurochem Res 32:707-15. 2007
    ..Abnormalities in mitochondria are associated with neurodegenerative and psychiatric disorders, suggesting a therapeutic potential for approaches that target mitochondrial mechanisms...
  53. ncbi Neuronal life-and-death signaling, apoptosis, and neurodegenerative disorders
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, Maryland 21224, USA
    Antioxid Redox Signal 8:1997-2006. 2006
    ..Emerging findings suggest that the resistance of neurons to death during aging can be enhanced by modifications of diet and lifestyle...
  54. ncbi Energy intake and amyotrophic lateral sclerosis
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    Neuromolecular Med 9:17-20. 2007
    ..One reason that motor neurons might be selectively vulnerable to low-energy diets is that they are unable to engage neuroprotective responses to energetic stress response involving the protein chaperones, such as, heat-shock protein-70...
  55. ncbi Calcium and neurodegeneration
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD, USA
    Aging Cell 6:337-50. 2007
    ....
  56. ncbi A lifetime of dedication to the old in his Kentucky home
    Mark P Mattson
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA
    Neuromolecular Med 13:6-10. 2011
    ..Also described below are the results of several research projects on which I had the good fortune of collaborating with Dr. Markesbery...
  57. 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
    ....
  58. ncbi Apoptosis in neurodegenerative disorders
    M P Mattson
    Laboratory of Neurosciences, National Institute on Aging, Gerontology Research Center, 5, 600 Nathan Shock Drive, Baltimore, Maryland 21224, USA
    Nat Rev Mol Cell Biol 1:120-9. 2000
    ..With the identification of mechanisms that either promote or prevent neuronal apoptosis come new approaches for preventing and treating neurodegenerative disorders...
  59. ncbi Suppression of brain aging and neurodegenerative disorders by dietary restriction and environmental enrichment: molecular mechanisms
    M P Mattson
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, 5600 Nathan Shock Drive, Baltimore, MD 21224 6825, USA
    Mech Ageing Dev 122:757-78. 2001
    ..A better understanding of the cellular and molecular mechanisms underlying these effects of diet and behavior on the brain is leading to novel therapeutic agents that mimick their beneficial effects...
  60. 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...
  61. ncbi Existing data suggest that Alzheimer's disease is preventable
    M P Mattson
    Laboratory of Neurosciences, National Institute on Aging, 5600 Nathan Shock Drive, Baltimore, Maryland 21224, USA
    Ann N Y Acad Sci 924:153-9. 2000
    ....
  62. ncbi Emerging neuroprotective strategies for Alzheimer's disease: dietary restriction, telomerase activation, and stem cell therapy
    M P Mattson
    Laboratory of Neurosciences 4F01, National Institute on Aging, 5600 Nathan Shock Drive, Baltimore, MD 23224, USA
    Exp Gerontol 35:489-502. 2000
    ..Finally, the exciting and exploding field of stem cell research suggests methods for replacing damaged or lost brain cells in an array of neurological disorders...
  63. ncbi Apoptotic and anti-apoptotic synaptic signaling mechanisms
    M P Mattson
    Laboratory of Neurosciences, National Institute on Aging, Baltimore, MD 21224, USA
    Brain Pathol 10:300-12. 2000
    ..A better understanding of such synaptic signaling mechanisms may reveal novel approaches for preventing and treating an array of neurodegenerative conditions that are initiated by perturbed synaptic homeostasis...
  64. ncbi Dysregulation of cellular calcium homeostasis in Alzheimer's disease: bad genes and bad habits
    M P Mattson
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, Baltimore, MD 21224, USA
    J Mol Neurosci 17:205-24. 2001
    ..The emerging picture of the cell and molecular biology of AD is revealing novel preventative and therapeutic strategies for eradicating this growing epidemic of the elderly...
  65. ncbi Emerging roles for telomerase in neuronal development and apoptosis
    M P Mattson
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, 4F02, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA
    J Neurosci Res 63:1-9. 2001
    ..J. Neurosci. Res. 63:1-9, 2001. Published 2001 Wiley-Liss, Inc...
  66. ncbi Neuroprotective signaling and the aging brain: take away my food and let me run
    M P Mattson
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, 5600 Nathan Shock Drive, 21224 6825, Baltimore, MD, USA
    Brain Res 886:47-53. 2000
    ....
  67. 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
    ....
  68. ncbi Apoptotic and antiapoptotic mechanisms in stroke
    M P Mattson
    Laboratory of Neurosciences, National Institute on Aging, Baltimore, MD 21224 6825, USA
    Cell Tissue Res 301:173-87. 2000
    ..Interestingly, recent studies suggest novel dietary approaches (e.g., food restriction and supplementation with antioxidants) that may reduce brain damage following stroke...
  69. 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...
  70. ncbi Neurodegenerative disorders and ischemic brain diseases
    M P Mattson
    Laboratory of Neurosciences, National Institute on Aging, Baltimore, MD 21224, USA
    Apoptosis 6:69-81. 2001
    ..A better understanding of the molecular underpinnings of neuronal death is leading directly to novel preventative and therapeutic approaches to neurodegenerative disorders...
  71. ncbi Presenilin mutations and calcium signaling defects in the nervous and immune systems
    M P Mattson
    Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, Baltimore, MD 21224, USA
    Bioessays 23:733-44. 2001
    ..A better understanding of the calcium signaling defect resulting from PS1 mutations may lead to the development of novel preventative and therapeutic strategies for disorders of the nervous and immune systems...
  72. ncbi 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...
  73. ncbi 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
    ....
  74. ncbi 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...
  75. ncbi 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...
  76. ncbi 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...
  77. ncbi 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...
  78. ncbi 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...
  79. ncbi 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...
  80. ncbi 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...
  81. ncbi 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...
  82. 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...
  83. ncbi 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...
  84. ncbi 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...
  85. ncbi 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...
  86. ncbi 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...
  87. ncbi 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...
  88. 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...
  89. ncbi 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
    ....
  90. ncbi 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...
  91. ncbi 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
    ....
  92. ncbi 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
    ....
  93. ncbi 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...
  94. ncbi 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...
  95. ncbi 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
    ....
  96. ncbi 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...
  97. ncbi 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...
  98. ncbi 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
  99. ncbi 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...
  100. 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...
  101. ncbi 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...