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The role of oxidative stress in the pathophysiology of cerebrovascular lesions in Alzheimer's disease.
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AD should be re-classified as an oxidative stress induced vascular disorder and described as a “vasocognopathy” with mitochondrial failure.
SHOW Details
Supporting(12)
Experimental Approach: Pathophysiology, Mechanism - physiological systems,
Pathogenic Narrative Tags: Pathologic change
Supporting Evidence
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Aliev G,
Smith M,
Obrenovich M,
de la Torre J,
Perry G
Role of vascular hypoperfusion-induced oxidative stress and mitochondria failure in the pathogenesis of Azheimer disease.
Neurotoxicity research. 2003;5(7):491-504 -
de la Torre J
Cerebrovascular gene linked to Alzheimer's disease pathology.
Trends in molecular medicine. 2005 Dec;11(12):534-6 -
de la Torre J,
Aliev G
Inhibition of vascular nitric oxide after rat chronic brain hypoperfusion: spatial memory and immunocytochemical changes.
Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism. 2005 Jun;25(6):663-72 -
de la Torre J
Vascular basis of Alzheimer's pathogenesis.
Annals of the New York Academy of Sciences. 2002 Nov;977:196-215 -
de la Torre J
Alzheimer's disease is a vasocognopathy: a new term to describe its nature.
Neurological research. 2004 Jul;26(5):517-24 -
de la Torre J
Is Alzheimer's disease a neurodegenerative or a vascular disorder? Data, dogma, and dialectics.
Lancet neurology. 2004 Mar;3(3):184-90 -
Aliev G,
Palacios H,
Walrafen B,
Lipsitt A,
Obrenovich M,
Morales L
Brain mitochondria as a primary target in the development of treatment strategies for Alzheimer disease.
The international journal of biochemistry & cell biology. 2009 Oct;41(10):1989-2004 -
Aliev G,
Palacios H,
Lipsitt A,
Fischbach K,
Lamb B,
Obrenovich M,
Morales L,
Gasimov E,
Bragin V
Nitric oxide as an initiator of brain lesions during the development of Alzheimer disease.
Neurotoxicity research. 2009 Oct;16(3):293-305 -
Hirai K,
Aliev G,
Nunomura A,
Fujioka H,
Russell R,
Atwood C,
Johnson A,
Kress Y,
Vinters H,
Tabaton M,
Shimohama S,
Cash A,
Siedlak S,
Harris P,
Jones P,
Petersen R,
Perry G,
Smith M
Mitochondrial abnormalities in Alzheimer's disease.
The Journal of neuroscience : the official journal of the Society for Neuroscience. 2001 May 1;21(9):3017-23 -
Obrenovich M,
Smith M,
Siedlak S,
Chen S,
de la Torre J,
Perry G,
Aliev G
Overexpression of GRK2 in Alzheimer disease and in a chronic hypoperfusion rat model is an early marker of brain mitochondrial lesions.
Neurotoxicity research. 2006 Aug;10(1):43-56 -
Obrenovich M,
Morales L,
Cobb C,
Shenk J,
Méndez G,
Fischbach K,
Smith M,
Qasimov E,
Perry G,
Aliev G
Insights into cerebrovascular complications and Alzheimer disease through the selective loss of GRK2 regulation.
Journal of cellular and molecular medicine. 2009 May;13(5):853-65 -
Aliev G,
Smith M,
Seyidov D,
Neal M,
Lamb B,
Nunomura A,
Gasimov E,
Vinters H,
Perry G,
LaManna J,
Friedland R
The role of oxidative stress in the pathophysiology of cerebrovascular lesions in Alzheimer's disease.
Brain pathology (Zurich, Switzerland). 2002 Jan;12(1):21-35
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The amyloid hypothesis has been criticized because its research findings up to now have not generated any benefits in the clinical management and treatment of AD patients nor to an understanding of how the elderly are preferentially affected.
SHOW Details Supporting(7)
Consistent(3)
Description: Additional sources of Supportive Evidence:Scientific and Clinical Frontiers in the Treatment of Alzheimer’s Disease: Identification of Novel Pathways and Development of New Treatments, PeerView Press, 2009
Experimental Approach: Pathophysiology, Clinical trials, Epidemiology, Target validation, Mechanism - biochemistry and structural biology
Pathogenic Narrative Tags: Pathologic change
Supporting Evidence
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de la Torre J
Pathophysiology of neuronal energy crisis in Alzheimer's disease.
Neuro-degenerative diseases. 2008;5(3-4):126-32 -
Aliev G,
Seyidova D,
Lamb B,
Obrenovich M,
Siedlak S,
Vinters H,
Friedland R,
LaManna J,
Smith M,
Perry G
Mitochondria and vascular lesions as a central target for the development of Alzheimer's disease and Alzheimer disease-like pathology in transgenic mice.
Neurological research. 2003 Sep;25(6):665-74 -
de la Torre J
Carotid artery ultrasound and echocardiography testing to lower the prevalence of Alzheimer's disease.
Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association. 2009;18(4):319-28 -
Aliev G,
Smith M,
Seyidov D,
Neal M,
Lamb B,
Nunomura A,
Gasimov E,
Vinters H,
Perry G,
LaManna J,
Friedland R
The role of oxidative stress in the pathophysiology of cerebrovascular lesions in Alzheimer's disease.
Brain pathology (Zurich, Switzerland). 2002 Jan;12(1):21-35 -
de la Torre J
Cerebrovascular and cardiovascular pathology in Alzheimer's disease.
International review of neurobiology. 2009;84:35-48 -
Aliev G,
Smith M,
Obrenovich M,
de la Torre J,
Perry G
Role of vascular hypoperfusion-induced oxidative stress and mitochondria failure in the pathogenesis of Azheimer disease.
Neurotoxicity research. 2003;5(7):491-504 -
Aliev G,
Obrenovich M,
Smith M,
Perry G
Hypoperfusion, Mitochondria Failure, Oxidative Stress, and Alzheimer Disease.
Journal of biomedicine & biotechnology. 2003;2003(3):162-163
Short-term clinical outcomes of the phase I AN1792 clinical trial were disappointing, with three of the four exploratory measures of clinical efficacy showing no significant differences between the treatment and placebo group during the initial study period.
Holmes C
Boche D
Wilkinson D
Yadegarfar G
Hopkins V
Bayer A
Jones R
Bullock R
Love S
Neal J
Zotova E
Nicoll J
Three “amyloid” hypothesis clinical trials including the active immunization trial, the passive immunization trial and γ-secretase modulator R-flurbuprofen (Tarenflurbil) trial, leave little certainty of clinical benefit, and that massively reducing amyloid burden late in the disease, is not a miracle cure.
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PubMed
