Hani Atamna

Summary

Affiliation: Children's Hospital Oakland Research Institute
Country: USA

Publications

  1. pmc Amyloid-beta peptide binds with heme to form a peroxidase: relationship to the cytopathologies of Alzheimer's disease
    Hani Atamna
    Nutrition and Metabolism Center, Children s Hospital Oakland Research Institute, CA 94609, USA
    Proc Natl Acad Sci U S A 103:3381-6. 2006
  2. ncbi request reprint Mechanisms of mitochondrial dysfunction and energy deficiency in Alzheimer's disease
    Hani Atamna
    Nutrition and Metabolism Center, Children s Hospital Oakland Research Institute, 5700 Martin Luther King Jr Way, Oakland, CA 94609 1673, USA
    Mitochondrion 7:297-310. 2007
  3. ncbi request reprint Heme binding to Amyloid-beta peptide: mechanistic role in Alzheimer's disease
    Hani Atamna
    Nutrition and Metabolism Center, Children s Hospital Oakland Research Institute CHORI, Oakland, CA 94609, USA
    J Alzheimers Dis 10:255-66. 2006
  4. ncbi request reprint Methylene blue delays cellular senescence and enhances key mitochondrial biochemical pathways
    Hani Atamna
    Nutrition and Metabolism Center, Children s Hospital Oakland Research Institute, 5700 Martin Luther King Jr Way, Oakland, CA 94609 1673, USA
    FASEB J 22:703-12. 2008
  5. pmc A role for heme in Alzheimer's disease: heme binds amyloid beta and has altered metabolism
    Hani Atamna
    Nutritional Genomics Center, Children s Hospital Oakland Research Institute, CA 94609, USA
    Proc Natl Acad Sci U S A 101:11153-8. 2004
  6. ncbi request reprint Heme, iron, and the mitochondrial decay of ageing
    Hani Atamna
    Children s Hospital Oakland Research Institute, 5700 Martin Luther King Jr Way, Oakland, CA 94609 1673, USA
    Ageing Res Rev 3:303-18. 2004
  7. pmc Heme deficiency may be a factor in the mitochondrial and neuronal decay of aging
    Hani Atamna
    Children s Hospital Oakland Research Institute, Oakland, CA 94609, USA
    Proc Natl Acad Sci U S A 99:14807-12. 2002
  8. ncbi request reprint Iron accumulation during cellular senescence
    David W Killilea
    Children s Hospital Oakland Research Institute, Oakland, California 94609, USA
    Ann N Y Acad Sci 1019:365-7. 2004
  9. ncbi request reprint Biotin deficiency inhibits heme synthesis and impairs mitochondria in human lung fibroblasts
    Hani Atamna
    Nutrition and Metabolism Center, Children s Hospital Oakland Research Institute, Oakland, CA 94609, USA
    J Nutr 137:25-30. 2007
  10. ncbi request reprint Mineral and vitamin deficiencies can accelerate the mitochondrial decay of aging
    Bruce N Ames
    Nutrition, Metabolisms and Genomics Center, Children s Hospital Oakland Research Institute, Oakland, CA 94609, U States
    Mol Aspects Med 26:363-78. 2005

Collaborators

Detail Information

Publications17

  1. pmc Amyloid-beta peptide binds with heme to form a peroxidase: relationship to the cytopathologies of Alzheimer's disease
    Hani Atamna
    Nutrition and Metabolism Center, Children s Hospital Oakland Research Institute, CA 94609, USA
    Proc Natl Acad Sci U S A 103:3381-6. 2006
    ..The relevance of the binding of regulatory heme with excessive Abeta for mitochondrial dysfunction and neurotoxicity and other cytopathologies of AD is discussed...
  2. ncbi request reprint Mechanisms of mitochondrial dysfunction and energy deficiency in Alzheimer's disease
    Hani Atamna
    Nutrition and Metabolism Center, Children s Hospital Oakland Research Institute, 5700 Martin Luther King Jr Way, Oakland, CA 94609 1673, USA
    Mitochondrion 7:297-310. 2007
    ..We further discuss how protecting mitochondria could confer resistance to oxidative and environmental insults. Therapies targeted at protecting mitochondria may improve the clinical outcome of AD patients...
  3. ncbi request reprint Heme binding to Amyloid-beta peptide: mechanistic role in Alzheimer's disease
    Hani Atamna
    Nutrition and Metabolism Center, Children s Hospital Oakland Research Institute CHORI, Oakland, CA 94609, USA
    J Alzheimers Dis 10:255-66. 2006
    ..Genetic, nutritional, and toxicological factors that influence heme metabolism will be discussed in relevance to AD...
  4. ncbi request reprint Methylene blue delays cellular senescence and enhances key mitochondrial biochemical pathways
    Hani Atamna
    Nutrition and Metabolism Center, Children s Hospital Oakland Research Institute, 5700 Martin Luther King Jr Way, Oakland, CA 94609 1673, USA
    FASEB J 22:703-12. 2008
    ..MB may be useful to delay mitochondrial dysfunction with aging and the decrease in complex IV in Alzheimer disease...
  5. pmc A role for heme in Alzheimer's disease: heme binds amyloid beta and has altered metabolism
    Hani Atamna
    Nutritional Genomics Center, Children s Hospital Oakland Research Institute, CA 94609, USA
    Proc Natl Acad Sci U S A 101:11153-8. 2004
    ..g., heme-a) and resulting in functional heme deficiency. The model integrates disparate observations, including A beta, mitochondrial dysfunction, cholesterol, and the proposed efficacy of clioquinol...
  6. ncbi request reprint Heme, iron, and the mitochondrial decay of ageing
    Hani Atamna
    Children s Hospital Oakland Research Institute, 5700 Martin Luther King Jr Way, Oakland, CA 94609 1673, USA
    Ageing Res Rev 3:303-18. 2004
    ..This review discusses heme metabolism as related to metabolic changes seen in ageing and age-related disorders and highlights the possible role in iron deficiency...
  7. pmc Heme deficiency may be a factor in the mitochondrial and neuronal decay of aging
    Hani Atamna
    Children s Hospital Oakland Research Institute, Oakland, CA 94609, USA
    Proc Natl Acad Sci U S A 99:14807-12. 2002
    ..Thus, heme deficiency or dysregulation may be an important and preventable component of the neurodegenerative process...
  8. ncbi request reprint Iron accumulation during cellular senescence
    David W Killilea
    Children s Hospital Oakland Research Institute, Oakland, California 94609, USA
    Ann N Y Acad Sci 1019:365-7. 2004
    ..Thus, iron accumulation is not a cause, but a consequence of normal cellular senescence in vitro. Senescence-associated iron accumulation may contribute to the increased oxidative stress and cellular dysfunction seen in senescent cells...
  9. ncbi request reprint Biotin deficiency inhibits heme synthesis and impairs mitochondria in human lung fibroblasts
    Hani Atamna
    Nutrition and Metabolism Center, Children s Hospital Oakland Research Institute, Oakland, CA 94609, USA
    J Nutr 137:25-30. 2007
    ..The findings are discussed in relation to aging and birth defects in humans...
  10. ncbi request reprint Mineral and vitamin deficiencies can accelerate the mitochondrial decay of aging
    Bruce N Ames
    Nutrition, Metabolisms and Genomics Center, Children s Hospital Oakland Research Institute, Oakland, CA 94609, U States
    Mol Aspects Med 26:363-78. 2005
    ..An optimum intake of micronutrients could tune up metabolism and give a marked increase in health, particularly for the poor, elderly, and obese, at little cost...
  11. ncbi request reprint Iron accumulation during cellular senescence in human fibroblasts in vitro
    David W Killilea
    Children s Hospital Oakland Research Institute, Oakland, CA 94609, USA
    Antioxid Redox Signal 5:507-16. 2003
    ..These data indicate that iron accumulation occurs during normal cellular senescence in vitro. This accumulation of iron may contribute to the increased oxidative stress and cellular dysfunction seen in senescent cells...
  12. ncbi request reprint Human and rodent amyloid-beta peptides differentially bind heme: relevance to the human susceptibility to Alzheimer's disease
    Hani Atamna
    Nutrition and Metabolism Center, Children s Hospital Oakland Research Institute, Oakland, CA 94609, USA
    Arch Biochem Biophys 487:59-65. 2009
    ..Phylogenic variations in the amino acid sequence of Abeta explain tight heme-binding to huAbeta and likely contribute to the increased human susceptibility to AD...
  13. pmc N-tert-butyl hydroxylamine, a mitochondrial antioxidant, protects human retinal pigment epithelial cells from iron overload: relevance to macular degeneration
    Ludmila A Voloboueva
    Children s Hospital Oakland Research Institute, Nutrition and Metabolism Center, 5700 Martin Luther King Jr Way, Oakland, CA 94609 1673, USA
    FASEB J 21:4077-86. 2007
    ..NtBHA might be useful in AMD due to its potential to reduce oxidative stress, mitochondrial damage, and age-related iron accumulation, which may damage normal RPE function and lead to loss of vision...
  14. ncbi request reprint The role of heme and iron-sulfur clusters in mitochondrial biogenesis, maintenance, and decay with age
    Hani Atamna
    Department of Molecular and Cell Biology, University of California, Berkeley CHORI, 5700 Martin Luther King Jr Way, Oakland, California 94609, USA
    Arch Biochem Biophys 397:345-53. 2002
    ..We review the physiological role of iron-sulfur clusters and heme in the integrity of the mitochondria and the generation of oxidants...
  15. pmc Deep sequencing reveals novel microRNAs and regulation of microRNA expression during cell senescence
    Joseph M Dhahbi
    Center for Genetics, Children s Hospital Oakland Research Institute, Oakland, California, United States of America
    PLoS ONE 6:e20509. 2011
    ..This result greatly extends existing information on the role of miRNAs in cell senescence and is consistent with miRNAs having a causal role in the process...
  16. ncbi request reprint Gender and age-dependent differences in the mitochondrial apoptogenic pathway in Alzheimer's disease
    Ana Lloret
    Departamento de Fisiologia, Facultad de Medicina, Avda Blasco Ibanez 15, 46010 Valencia, Spain
    Free Radic Biol Med 44:2019-25. 2008
    ..Gender and age-related differences seen in the development of AD can also be partially explained...
  17. ncbi request reprint Delaying brain mitochondrial decay and aging with mitochondrial antioxidants and metabolites
    Jiankang Liu
    Division of Biochemistry and Molecular Biology, University of California, Berkeley, California 94720, USA
    Ann N Y Acad Sci 959:133-66. 2002
    ..This loss of activity due to coenzyme or substrate binding appears to be true for a number of other enzymes as well, including mitochondrial complex III and IV...