G Aliev

Summary

Affiliation: University of Texas at San Antonio
Country: USA

Publications

  1. ncbi request reprint Ultrastructural analysis of a murine model of congenital hydrocephalus produced by overexpression of transforming growth factor-beta1 in the central nervous system
    G Aliev
    Department of Biology, College of Sciences, The University of Texas at San Antonio, TX 78249 0661, USA
    J Submicrosc Cytol Pathol 38:85-91. 2006
  2. pmc Atherosclerotic lesions and mitochondria DNA deletions in brain microvessels: implication in the pathogenesis of Alzheimer's disease
    Gjumrakch Aliev
    Department of Biology, University of Texas at San Antonio, San Antonio, Texas 78249 1664, USA
    Vasc Health Risk Manag 4:721-30. 2008
  3. pmc Neuronal mitochondrial amelioration by feeding acetyl-L-carnitine and lipoic acid to aged rats
    Gjumrakch Aliev
    Department of Biology, University of Texas at San Antonio, 78249, USA
    J Cell Mol Med 13:320-33. 2009
  4. doi request reprint Stem cell niches as clinical targets: the future of anti-ischemic therapy?
    Gjumrakch Aliev
    Department of Biology, University of Texas at San Antonio, San Antonio, TX 78249 1664, USA
    Nat Clin Pract Cardiovasc Med 5:590-1. 2008
  5. ncbi request reprint Role of mitochondrial dysfunction in Alzheimer's disease
    Rudy Castellani
    Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    J Neurosci Res 70:357-60. 2002
  6. ncbi request reprint Atherosclerotic lesions and mitochondria DNA deletions in brain microvessels as a central target for the development of human AD and AD-like pathology in aged transgenic mice
    Gjumrakch Aliev
    Microscopy Research Center, Department of Anatomy, Case Western Reserve University and University Hospitals of Cleveland, 2085 Adelbert Road, Cleveland, OH 44106, USA
    Ann N Y Acad Sci 977:45-64. 2002
  7. pmc Microtubule reduction in Alzheimer's disease and aging is independent of tau filament formation
    Adam D Cash
    Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    Am J Pathol 162:1623-7. 2003
  8. ncbi request reprint Mitochondria and vascular lesions as a central target for the development of Alzheimer's disease and Alzheimer disease-like pathology in transgenic mice
    Gjumrakch Aliev
    Microscopy Research Center, Department of Anatomy, Department of Pathology, Case Western Reserve University, University Hospitals of Cleveland, Cleveland, OH, USA
    Neurol Res 25:665-74. 2003
  9. ncbi request reprint Mitochondria DNA deletions in atherosclerotic hypoperfused brain microvessels as a primary target for the development of Alzheimer's disease
    Ali Aliyev
    The Microscopy Research Center, Case Western Reserve University, Cleveland, OH 44106, USA
    J Neurol Sci 229:285-92. 2005
  10. ncbi request reprint Oxidative damage and Alzheimer's disease: are antioxidant therapies useful?
    Paula I Moreira
    Institute of Pathology, Case Western Research University, Cleveland, OH 44106, USA
    Drug News Perspect 18:13-9. 2005

Collaborators

Detail Information

Publications32

  1. ncbi request reprint Ultrastructural analysis of a murine model of congenital hydrocephalus produced by overexpression of transforming growth factor-beta1 in the central nervous system
    G Aliev
    Department of Biology, College of Sciences, The University of Texas at San Antonio, TX 78249 0661, USA
    J Submicrosc Cytol Pathol 38:85-91. 2006
    ..Our results suggest that congenital hydrocephalus may be associated with significant damage to cortical tissue...
  2. pmc Atherosclerotic lesions and mitochondria DNA deletions in brain microvessels: implication in the pathogenesis of Alzheimer's disease
    Gjumrakch Aliev
    Department of Biology, University of Texas at San Antonio, San Antonio, Texas 78249 1664, USA
    Vasc Health Risk Manag 4:721-30. 2008
    ..Therefore, pharmacological interventions, directed at correcting the chronic hypoperfusion state, may change the natural course of the development of dementing neurodegeneration...
  3. pmc Neuronal mitochondrial amelioration by feeding acetyl-L-carnitine and lipoic acid to aged rats
    Gjumrakch Aliev
    Department of Biology, University of Texas at San Antonio, 78249, USA
    J Cell Mol Med 13:320-33. 2009
    ..001) in the hippocampus. These results suggest that feeding ALCAR with LA may ameliorate age-associated mitochondrial ultrastructural decay and are consistent with previous studies showing improved brain function...
  4. doi request reprint Stem cell niches as clinical targets: the future of anti-ischemic therapy?
    Gjumrakch Aliev
    Department of Biology, University of Texas at San Antonio, San Antonio, TX 78249 1664, USA
    Nat Clin Pract Cardiovasc Med 5:590-1. 2008
    ..Further assessment is needed to elucidate the factors involved in migration and differentiation of endothelial cell progenitors in ischemia-damaged tissues...
  5. ncbi request reprint Role of mitochondrial dysfunction in Alzheimer's disease
    Rudy Castellani
    Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    J Neurosci Res 70:357-60. 2002
    ..Here we review the causes and consequences of mitochondrial disturbances in Alzheimer's disease as well as how this information might impact on therapeutic approaches to this disease...
  6. ncbi request reprint Atherosclerotic lesions and mitochondria DNA deletions in brain microvessels as a central target for the development of human AD and AD-like pathology in aged transgenic mice
    Gjumrakch Aliev
    Microscopy Research Center, Department of Anatomy, Case Western Reserve University and University Hospitals of Cleveland, 2085 Adelbert Road, Cleveland, OH 44106, USA
    Ann N Y Acad Sci 977:45-64. 2002
    ..Our observations demonstrate that vascular wall cells, especially their mitochondria, appear to be a central target for oxidative stress-induced damage...
  7. pmc Microtubule reduction in Alzheimer's disease and aging is independent of tau filament formation
    Adam D Cash
    Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    Am J Pathol 162:1623-7. 2003
    ..016). These findings suggest that reduction in microtubule assembly is not dependent on tau abnormalities of AD and aging...
  8. ncbi request reprint Mitochondria and vascular lesions as a central target for the development of Alzheimer's disease and Alzheimer disease-like pathology in transgenic mice
    Gjumrakch Aliev
    Microscopy Research Center, Department of Anatomy, Department of Pathology, Case Western Reserve University, University Hospitals of Cleveland, Cleveland, OH, USA
    Neurol Res 25:665-74. 2003
    ..Our observations first time demonstrate that vascular wall cells, especially their mitochondria, appear to be a central target for oxidative stress induced damage...
  9. ncbi request reprint Mitochondria DNA deletions in atherosclerotic hypoperfused brain microvessels as a primary target for the development of Alzheimer's disease
    Ali Aliyev
    The Microscopy Research Center, Case Western Reserve University, Cleveland, OH 44106, USA
    J Neurol Sci 229:285-92. 2005
    ..Therefore, selective pharmacological intervention, directed for abolishing the chronic hypoperfusion state, would possibly change the natural course of development of dementing neurodegeneration...
  10. ncbi request reprint Oxidative damage and Alzheimer's disease: are antioxidant therapies useful?
    Paula I Moreira
    Institute of Pathology, Case Western Research University, Cleveland, OH 44106, USA
    Drug News Perspect 18:13-9. 2005
    ..However, the results obtained in clinical trials with antioxidants are promising and propel us in the search of new and more effective antioxidant therapies...
  11. ncbi request reprint Oxidative stress: the old enemy in Alzheimer's disease pathophysiology
    Paula I Moreira
    Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    Curr Alzheimer Res 2:403-8. 2005
    ....
  12. ncbi request reprint Mitochondrial abnormalities and oxidative imbalance in Alzheimer disease
    Xiongwei Zhu
    Department of Pathology, Case Western Reserve University, 2103 Cornell Road, Cleveland, Ohio 44106, USA
    J Alzheimers Dis 9:147-53. 2006
    ....
  13. ncbi request reprint Overexpression of GRK2 in Alzheimer disease and in a chronic hypoperfusion rat model is an early marker of brain mitochondrial lesions
    Mark E Obrenovich
    Department of Pathology, School of Medicine, Case Western Reserve University, Cleveland, OH 44106, USA
    Neurotox Res 10:43-56. 2006
    ....
  14. pmc Vascular oxidative stress in Alzheimer disease
    Xiongwei Zhu
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    J Neurol Sci 257:240-6. 2007
    ..Here, we discuss vascular factors in relation to Alzheimer disease and review hypoperfusion as a potential cause by triggering mitochondrial dysfunction and increased oxidative stress initiating the pathogenic process...
  15. ncbi request reprint Autophagocytosis of mitochondria is prominent in Alzheimer disease
    Paula I Moreira
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio, USA
    J Neuropathol Exp Neurol 66:525-32. 2007
    ..Whether increased autophagocytosis is a consequence of an increased turnover of mitochondria or whether the mitochondria in Alzheimer disease are more susceptible to autophagy remains to be resolved...
  16. ncbi request reprint Increased autophagic degradation of mitochondria in Alzheimer disease
    Paula I Moreira
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio, USA
    Autophagy 3:614-5. 2007
    ..The study of autophagy in Alzheimer disease could clarify the mechanisms underlying this neurodegenerative disorder and, eventually, help in the development of new therapeutic strategies...
  17. doi request reprint Nucleic acid oxidation in Alzheimer disease
    Paula I Moreira
    Center for Neuroscience and Cell Biology, Institute of Physiology Faculty of Medicine, University of Coimbra, Coimbra, Portugal
    Free Radic Biol Med 44:1493-505. 2008
    ..Furthermore, we outline the mechanisms of nucleic acid oxidation and repair. Finally, evidence showing the occurrence of nucleic acid oxidation in Alzheimer disease will be discussed...
  18. ncbi request reprint Integrated treatment approach improves cognitive function in demented and clinically depressed patients
    Valentin Bragin
    Stress Relief and Memory Training Center, Brooklyn, New York, USA
    Am J Alzheimers Dis Other Demen 20:21-6. 2005
    ..Results show that the integrative treatment not only protracted cognitive decline for 24 months but even improved cognition, especially memory and frontal lobe functions...
  19. ncbi request reprint Alzheimer-specific epitopes of tau represent lipid peroxidation-induced conformations
    Quan Liu
    Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA
    Free Radic Biol Med 38:746-54. 2005
    ....
  20. ncbi request reprint Labeling of cerebral amyloid beta deposits in vivo using intranasal basic fibroblast growth factor and serum amyloid P component in mice
    Jiong Shi
    Department of Neurology, Case Western Reserve University, University Hospitals of Cleveland, Ohio 44106 4962, USA
    J Nucl Med 43:1044-51. 2002
    ....
  21. ncbi request reprint Is oxidative damage the fundamental pathogenic mechanism of Alzheimer's and other neurodegenerative diseases?
    George Perry
    Institute of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA
    Free Radic Biol Med 33:1475-9. 2002
    ..Although much data remain to be collected, the broad spectrum of changes found in AD are only seen, albeit to a lesser extent, in normal aging with other neurodegenerative diseases showing distinct spectrums of change...
  22. ncbi request reprint Is non-genetic Alzheimer's disease a vascular disorder with neurodegenerative consequences?
    Gjumrakch Aliev
    Microscopy Research Center, Institute of Pathology, Case Western Reserve University, Celeveland, OH 44106, USA
    J Alzheimers Dis 4:513-6. 2002
  23. ncbi request reprint A metabolic basis for Alzheimer disease
    George Perry
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    Neurochem Res 28:1549-52. 2003
    ..Here we present data indicating that metabolic rate, nutrition, and neuronal size are all early indicators of AD. Understanding the cellular and molecular basis for these changes may open a new dimension to understanding AD...
  24. ncbi request reprint Will preventing protein aggregates live up to its promise as prophylaxis against neurodegenerative diseases?
    Hyoung gon Lee
    Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    Brain Pathol 13:630-8. 2003
    ..In this review, we weigh the evidence of whether removal of amyloids, aggregates and neuronal inclusions represent a reasonable strategy for protecting neurons...
  25. ncbi request reprint Role of vascular hypoperfusion-induced oxidative stress and mitochondria failure in the pathogenesis of Azheimer disease
    Gjumrakch Aliev
    The Microscopy Research Center and Department of Pathology, School of Medicine, Case Western Reserve University, Cleveland OH 44106, USA
    Neurotox Res 5:491-504. 2003
    ....
  26. ncbi request reprint Alzheimer disease: evidence for a central pathogenic role of iron-mediated reactive oxygen species
    Gemma Casadesus
    Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    J Alzheimers Dis 6:165-9. 2004
    ..In this review, we consider the wealth of evidence implicating a central role for metals in Alzheimer disease...
  27. ncbi request reprint Is nitric oxide a key target in the pathogenesis of brain lesions during the development of Alzheimer's disease?
    Ali Aliyev
    Microscopy Research Center, Case Western Reserve University, Cleveland, OH 44106, USA
    Neurol Res 26:547-53. 2004
    ..We speculate that pharmacological intervention using NO donors and/or NO suppressors will be able to delay or minimize the development of brain pathology and further progression of mental retardation...
  28. ncbi request reprint The role of nitric oxide in the pathogenesis of brain lesions during the development of Alzheimer's disease
    Dilara Seyidova
    Microscopy Research Center, Institute of Pathology, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106, USA
    In Vivo 18:325-33. 2004
    ..We theorize that pharmacological intervention using NO donors and/or NO suppressors should delay or minimize brain lesion development and further progression of brain pathology and dementia...
  29. ncbi request reprint Drug therapy in Alzheimer's disease
    Jack de la Torre
    N Engl J Med 351:1911-3; author reply 1911-3. 2004
  30. ncbi request reprint Mitochondrial failures in Alzheimer's disease
    Xiongwei Zhu
    Institute of Pathology, Case Western Reserve University, Cleveland, Ohio, USA
    Am J Alzheimers Dis Other Demen 19:345-52. 2004
    ..Future studies comparing the spectrum of mitochondrial damage and the relationship to oxidative stress-induced damage during the aging process or, more importantly, during the maturation of AD pathology are warranted...
  31. ncbi request reprint Inhibition of vascular nitric oxide after rat chronic brain hypoperfusion: spatial memory and immunocytochemical changes
    Jack C de la Torre
    1Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    J Cereb Blood Flow Metab 25:663-72. 2005
    ..These findings may identify therapeutic targets for preventing MCI and treating Alzheimer's disease...
  32. ncbi request reprint The role of oxidative stress in the pathophysiology of cerebrovascular lesions in Alzheimer's disease
    Gjumrakch Aliev
    Electron Microscopy Center, and Department of Anatomy, Case Western Reserve University, School of Medicine and University Hospital of the Cleveland, OH 44106 4938, USA
    Brain Pathol 12:21-35. 2002
    ..We also consider the opportunities for therapeutic interventions based on the molecular pathways involved with these causal relationships...