Research Topics
| G AlievSummaryAffiliation: University of Texas at San Antonio Country: USA Publications
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Detail Information
Publications
Atherosclerotic lesions and mitochondria DNA deletions in brain microvessels: implication in the pathogenesis of Alzheimer's diseaseGjumrakch 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...
Ultrastructural analysis of a murine model of congenital hydrocephalus produced by overexpression of transforming growth factor-beta1 in the central nervous systemG 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...- Neuronal mitochondrial amelioration by feeding acetyl-L-carnitine and lipoic acid to aged ratsGjumrakch 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... 
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...- Role of mitochondrial dysfunction in Alzheimer's diseaseRudy 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... - 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 miceGjumrakch 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... - Microtubule reduction in Alzheimer's disease and aging is independent of tau filament formationAdam 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... - Mitochondria and vascular lesions as a central target for the development of Alzheimer's disease and Alzheimer disease-like pathology in transgenic miceGjumrakch 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... - Mitochondria DNA deletions in atherosclerotic hypoperfused brain microvessels as a primary target for the development of Alzheimer's diseaseAli 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... - 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... - Oxidative stress: the old enemy in Alzheimer's disease pathophysiologyPaula I Moreira
Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
Curr Alzheimer Res 2:403-8. 2005.... - Mitochondrial abnormalities and oxidative imbalance in Alzheimer diseaseXiongwei Zhu
Department of Pathology, Case Western Reserve University, 2103 Cornell Road, Cleveland, Ohio 44106, USA
J Alzheimers Dis 9:147-53. 2006.... - Overexpression of GRK2 in Alzheimer disease and in a chronic hypoperfusion rat model is an early marker of brain mitochondrial lesionsMark E Obrenovich
Department of Pathology, School of Medicine, Case Western Reserve University, Cleveland, OH 44106, USA
Neurotox Res 10:43-56. 2006.... - Vascular oxidative stress in Alzheimer diseaseXiongwei 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... - Autophagocytosis of mitochondria is prominent in Alzheimer diseasePaula 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... - Increased autophagic degradation of mitochondria in Alzheimer diseasePaula 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... - Nucleic acid oxidation in Alzheimer diseasePaula 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... - Integrated treatment approach improves cognitive function in demented and clinically depressed patientsValentin 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... - Alzheimer-specific epitopes of tau represent lipid peroxidation-induced conformationsQuan Liu
Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106, USA
Free Radic Biol Med 38:746-54. 2005.... - Labeling of cerebral amyloid beta deposits in vivo using intranasal basic fibroblast growth factor and serum amyloid P component in miceJiong Shi
Department of Neurology, Case Western Reserve University, University Hospitals of Cleveland, Ohio 44106-4962, USA
J Nucl Med 43:1044-51. 2002..CONCLUSION: We report a novel noninvasive method for labeling Abeta plaques. This method may be modified for human studies using intranasal injection of radiolabeled ligands and imaging with SPECT or PET... - 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... - 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 - A metabolic basis for Alzheimer diseaseGeorge 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... - 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... - Role of vascular hypoperfusion-induced oxidative stress and mitochondria failure in the pathogenesis of Azheimer diseaseGjumrakch 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.... - Alzheimer disease: evidence for a central pathogenic role of iron-mediated reactive oxygen speciesGemma 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... - 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... - The role of nitric oxide in the pathogenesis of brain lesions during the development of Alzheimer's diseaseDilara 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... - Drug therapy in Alzheimer's diseaseJack de la Torre
N Engl J Med 351:1911-3; author reply 1911-3. 2004 - Mitochondrial failures in Alzheimer's diseaseXiongwei 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... - Inhibition of vascular nitric oxide after rat chronic brain hypoperfusion: spatial memory and immunocytochemical changesJack 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... - The role of oxidative stress in the pathophysiology of cerebrovascular lesions in Alzheimer's diseaseGjumrakch 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...