Gjumrakch Aliev

Summary

Publications

  1. ncbi request reprint Oxidative stress induced mitochondrial DNA deletion as a hallmark for the drug development in the context of the cerebrovascular diseases
    Gjumrakch Aliev
    School of Health Science and Healthcare Administration, University of Atlanta, Atlanta, Georgia 30360, USA
    Recent Pat Cardiovasc Drug Discov 6:222-41. 2011
  2. ncbi request reprint Oxidative stress mediated mitochondrial and vascular lesions as markers in the pathogenesis of Alzheimer disease
    G Aliev
    GALLY International Biomedical Research Consulting LLC, 7733 Louis Pasteur Drive, 330 San Antonio, TX, 78229, USA
    Curr Med Chem 21:2208-17. 2014
  3. pmc The GRK2 Overexpression Is a Primary Hallmark of Mitochondrial Lesions during Early Alzheimer Disease
    Mark E Obrenovich
    Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA
    Cardiovasc Psychiatry Neurol 2009:327360. 2009
  4. ncbi request reprint Pathogenesis of Alzheimer disease: role of oxidative stress, amyloid-β peptides, systemic ammonia and erythrocyte energy metabolism
    Elena A Kosenko
    GALLY International Biomedical Research Institute Inc, 7733 Louis Pasteur Drive, 328, San Antonio, TX, 78229, USA
    CNS Neurol Disord Drug Targets 13:112-9. 2014
  5. pmc Link between cancer and Alzheimer disease via oxidative stress induced by nitric oxide-dependent mitochondrial DNA overproliferation and deletion
    Gjumrakch Aliev
    GALLY International Biomedical Research Consulting LLC, 7733 Louis Pasteur Drive, No 328, San Antonio, TX 78229, USA
    Oxid Med Cell Longev 2013:962984. 2013
  6. doi request reprint Nitric oxide as an initiator of brain lesions during the development of Alzheimer disease
    Gjumrakch Aliev
    Department of Biology and Electron Microscopy Research Center, University of Texas at San Antonio, San Antonio, TX 78249, USA
    Neurotox Res 16:293-305. 2009
  7. doi request reprint Brain mitochondria as a primary target in the development of treatment strategies for Alzheimer disease
    Gjumrakch Aliev
    Department of Biology, College of Sciences, University of Texas at San Antonio, San Antonio, TX 78249, USA
    Int J Biochem Cell Biol 41:1989-2004. 2009
  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. 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
  10. ncbi request reprint Antioxidants in health, disease and aging
    Mark E Obrenovich
    Department of Chemistry, Cleveland State University, 2121 Euclid Ave SR 397B, Cleveland, OH 44115, USA
    CNS Neurol Disord Drug Targets 10:192-207. 2011

Collaborators

Detail Information

Publications45

  1. ncbi request reprint Oxidative stress induced mitochondrial DNA deletion as a hallmark for the drug development in the context of the cerebrovascular diseases
    Gjumrakch Aliev
    School of Health Science and Healthcare Administration, University of Atlanta, Atlanta, Georgia 30360, USA
    Recent Pat Cardiovasc Drug Discov 6:222-41. 2011
    ..Future potential exploration using mtDNA markers can be considered more accurate hallmarks for diagnosis and monitoring treatment of human diseases. The present article discusses some of the patents regarding the oxidative stress...
  2. ncbi request reprint Oxidative stress mediated mitochondrial and vascular lesions as markers in the pathogenesis of Alzheimer disease
    G Aliev
    GALLY International Biomedical Research Consulting LLC, 7733 Louis Pasteur Drive, 330 San Antonio, TX, 78229, USA
    Curr Med Chem 21:2208-17. 2014
    ..Delineating the molecular mechanisms of these processes may provide clues for the novel therapeutic targets for CVA and AD patients. ..
  3. pmc The GRK2 Overexpression Is a Primary Hallmark of Mitochondrial Lesions during Early Alzheimer Disease
    Mark E Obrenovich
    Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA
    Cardiovasc Psychiatry Neurol 2009:327360. 2009
    ....
  4. ncbi request reprint Pathogenesis of Alzheimer disease: role of oxidative stress, amyloid-β peptides, systemic ammonia and erythrocyte energy metabolism
    Elena A Kosenko
    GALLY International Biomedical Research Institute Inc, 7733 Louis Pasteur Drive, 328, San Antonio, TX, 78229, USA
    CNS Neurol Disord Drug Targets 13:112-9. 2014
    ....
  5. pmc Link between cancer and Alzheimer disease via oxidative stress induced by nitric oxide-dependent mitochondrial DNA overproliferation and deletion
    Gjumrakch Aliev
    GALLY International Biomedical Research Consulting LLC, 7733 Louis Pasteur Drive, No 328, San Antonio, TX 78229, USA
    Oxid Med Cell Longev 2013:962984. 2013
    ....
  6. doi request reprint Nitric oxide as an initiator of brain lesions during the development of Alzheimer disease
    Gjumrakch Aliev
    Department of Biology and Electron Microscopy Research Center, University of Texas at San Antonio, San Antonio, TX 78249, USA
    Neurotox Res 16:293-305. 2009
    ....
  7. doi request reprint Brain mitochondria as a primary target in the development of treatment strategies for Alzheimer disease
    Gjumrakch Aliev
    Department of Biology, College of Sciences, University of Texas at San Antonio, San Antonio, TX 78249, USA
    Int J Biochem Cell Biol 41:1989-2004. 2009
    ....
  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. 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...
  10. ncbi request reprint Antioxidants in health, disease and aging
    Mark E Obrenovich
    Department of Chemistry, Cleveland State University, 2121 Euclid Ave SR 397B, Cleveland, OH 44115, USA
    CNS Neurol Disord Drug Targets 10:192-207. 2011
    ....
  11. pmc Hydroxynonenal-generated crosslinking fluorophore accumulation in Alzheimer disease reveals a dichotomy of protein turnover
    Xiongwei Zhu
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    Free Radic Biol Med 52:699-704. 2012
    ..These findings directly implicate lipid crosslinking peroxidation products as accumulating not in the lesions or the lipofuscin pathways, but instead in a distinct pathway, GVD, that accumulates cytosolic proteins...
  12. pmc The effect of acetyl-L-carnitine and R-alpha-lipoic acid treatment in ApoE4 mouse as a model of human Alzheimer's disease
    Justin C Shenk
    Department of Biology and Electron Microscopy Research Center, University of Texas at San Antonio, San Antonio, TX 78249, USA
    J Neurol Sci 283:199-206. 2009
    ..Our findings indicate that ApoE4 genotype-induced mitochondrial changes and associated structural damage may explain age-dependent pathology seen in AD, indicating potential for novel treatment strategies in the near future...
  13. 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...
  14. 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...
  15. 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...
  16. 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...
  17. 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...
  18. 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...
  19. pmc Antioxidant therapy in Alzheimer's disease: theory and practice
    Gjumrakch Aliev
    Department of Biology, University of Texas at San Antonio, One UTSA Circle, San Antonio, Texas 78249, USA
    Mini Rev Med Chem 8:1395-406. 2008
    ..Efforts to reduce the pathology associated with ROS via antioxidants therefore offer new hope to patients suffering from this devastative disease...
  20. 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
    ....
  21. 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
    ....
  22. 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...
  23. 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...
  24. 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...
  25. 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...
  26. 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
    ....
  27. pmc Insights into cerebrovascular complications and Alzheimer disease through the selective loss of GRK2 regulation
    Mark E Obrenovich
    Department of Pathology, Case Western Reserve University, Cleveland, OH, USA
    J Cell Mol Med 13:853-65. 2009
    ..We synthesize this newer information and attempt to put it into context with GRKs as regulators of diverse physiological cellular functions that could be appropriate targets for future pharmacological intervention...
  28. 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
    ....
  29. 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...
  30. ncbi request reprint Antioxidant status and energy state of erythrocytes in Alzheimer dementia: probing for markers
    Elena A Kosenko
    GALLY International Biomedical Research Consulting LLC, 7733 Louis Pasteur Drive No 328, San Antonio, TX 78229 USA
    CNS Neurol Disord Drug Targets 11:926-32. 2012
    ..Decreased glutathione peroxidase activity in RBC may be considered as a new peripheral marker for AD...
  31. ncbi request reprint Mitochondrion-specific antioxidants as drug treatments for Alzheimer disease
    Hector H Palacios
    Department of Biology, College of Sciences, The University of Texas at San Antonio, One UTSA Circle, San Antonio, TX 78249 1664, USA
    CNS Neurol Disord Drug Targets 10:149-62. 2011
    ....
  32. 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...
  33. 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
    ....
  34. 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...
  35. 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...
  36. ncbi 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...
  37. 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...
  38. 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...
  39. 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...
  40. 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
    ....
  41. 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
  42. doi request reprint The role of polyphenolic antioxidants in health, disease, and aging
    Mark E Obrenovich
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    Rejuvenation Res 13:631-43. 2010
    ....
  43. 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...
  44. ncbi request reprint Effects of coenzyme Q and creatine supplementation on brain energy metabolism in rats exposed to chronic cerebral hypoperfusion
    Jaromír Horecký
    Surgical Pathophysiology and Tissue Engineering Center, Slovak Medical University, Bratislava, Slovak Republic
    Curr Alzheimer Res 8:868-75. 2011
    ..05) and γ-tocopherol in plasma. This suggests that coenzyme Q10 therapy involves resistance to oxidative stress and improved brain bioenergetics, when supplemented during reperfusion after ischemic brain injury...
  45. doi request reprint Implication of the nutritional and nonnutritional factors in the context of preservation of cognitive performance in patients with dementia/depression and Alzheimer disease
    Gjumrakch Aliev
    1GALLY International Biomedical Research Consulting LLC, San Antonio, TX, USA
    Am J Alzheimers Dis Other Demen 28:660-70. 2013
    ....