Role of vascular hypoperfusion-induced oxidative stress and mitochondria failure in the pathogenesis of Alzheimer disease

2003 ◽  
Vol 5 (7) ◽  
pp. 491-504 ◽  
Author(s):  
Gjumrakch Aliev ◽  
Mark A. Smith ◽  
Mark E. Obrenovich ◽  
Jack C. de la Torre ◽  
George Perry
Keyword(s):  
Oxidative Stress ◽  
Alzheimer Disease ◽  
Vascular Hypoperfusion

Pathogenesis of Alzheimer Disease: Role of Oxidative Stress, Amyloid-β Peptides, Systemic Ammonia and Erythrocyte Energy Metabolism

2014 ◽  
Vol 13 (1) ◽  
pp. 112-119 ◽  
Author(s):  
Elena Kosenko ◽  
Iliya Solomadin ◽  
Lyudmila Tikhonova ◽  
V. Reddy ◽  
Gjumrakch Aliev ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Energy Metabolism ◽  
Alzheimer Disease

scholarly journals Oxidative Stress Induced Mitochondrial Failure and Vascular Hypoperfusion as a Key Initiator for the Development of Alzheimer Disease

2010 ◽  
Vol 3 (1) ◽  
pp. 158-187 ◽  
Author(s):  
Gjumrakch Aliev ◽  
Hector Palacios ◽  
Eldar Gasimov ◽  
Mark Obrenovich ◽  
Ludis Morales ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer Disease ◽  
Vascular Hypoperfusion

VASCULAR HYPOPERFUSION AND MITOCHONDRIA ABNORMALITY INDUCE OXIDATIVE STRESS THAT APPEARED TO BE A KEY FACTOR FOR THE DEVELOPMENT OF ALZHEIMER DISEASE

2004 ◽  
Vol 13 (3) ◽  
pp. 26-27
Author(s):  
Gjumrakch Aliev ◽  
Dilara Seyidova ◽  
Mark A Smith ◽  
George Perry ◽  
Jack C de la Torre
Keyword(s):  
Oxidative Stress ◽  
Alzheimer Disease ◽  
Key Factor ◽  
Vascular Hypoperfusion

scholarly journals It Is All about (U)biquitin: Role of Altered Ubiquitin-Proteasome System and UCHL1 in Alzheimer Disease

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Antonella Tramutola ◽  
Fabio Di Domenico ◽  
Eugenio Barone ◽  
Marzia Perluigi ◽  
D. Allan Butterfield
Keyword(s):  
Oxidative Stress ◽  
Alzheimer Disease ◽  
Ubiquitin Proteasome System ◽  
Oxidative Modification ◽  
Age Related ◽  
Ubiquitin Proteasome ◽  
Proteasome Pathway ◽  
And Function ◽  
Cellular Components

Free radical-mediated damage to macromolecules and the resulting oxidative modification of different cellular components are a common feature of aging, and this process becomes much more pronounced in age-associated pathologies, including Alzheimer disease (AD). In particular, proteins are particularly sensitive to oxidative stress-induced damage and these irreversible modifications lead to the alteration of protein structure and function. In order to maintain cell homeostasis, these oxidized/damaged proteins have to be removed in order to prevent their toxic accumulation. It is generally accepted that the age-related accumulation of “aberrant” proteins results from both the increased occurrence of damage and the decreased efficiency of degradative systems. One of the most important cellular proteolytic systems responsible for the removal of oxidized proteins in the cytosol and in the nucleus is the proteasomal system. Several studies have demonstrated the impairment of the proteasome in AD thus suggesting a direct link between accumulation of oxidized/misfolded proteins and reduction of this clearance system. In this review we discuss the impairment of the proteasome system as a consequence of oxidative stress and how this contributes to AD neuropathology. Further, we focus the attention on the oxidative modifications of a key component of the ubiquitin-proteasome pathway, UCHL1, which lead to the impairment of its activity.

Oxidative Stress and Neuronal Adaptation in Alzheimer Disease: The Role of SAPK Pathways

2003 ◽  
Vol 5 (5) ◽  
pp. 571-576 ◽  
Author(s):  
Xiongwei Zhu ◽  
Arun K. Raina ◽  
Hyoung-Gon Lee ◽  
Mark Chao ◽  
Akihiko Nunomura ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer Disease ◽  
Neuronal Adaptation
Sign in / Sign up

Export Citation Format

Share Document