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Gjumrakch Aliev

Researcher at I.M. Sechenov First Moscow State Medical University

Publications -  277
Citations -  15215

Gjumrakch Aliev is an academic researcher from I.M. Sechenov First Moscow State Medical University. The author has contributed to research in topics: Oxidative stress & Alzheimer's disease. The author has an hindex of 48, co-authored 274 publications receiving 13202 citations. Previous affiliations of Gjumrakch Aliev include University of Arizona & Case Western Reserve University.

Papers
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Guidelines for the use and interpretation of assays for monitoring autophagy in higher eukaryotes

Daniel J. Klionsky, +235 more
- 16 Feb 2008 - 
TL;DR: A set of guidelines for the selection and interpretation of the methods that can be used by investigators who are attempting to examine macroautophagy and related processes, as well as by reviewers who need to provide realistic and reasonable critiques of papers that investigate these processes are presented.
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Oxidative damage is the earliest event in Alzheimer disease.

TL;DR: The observations indicate that increased oxidative damage is an early event in AD that decreases with disease progression and lesion formation and suggest that AD is associated with compensatory changes that reduce damage from reactive oxygen.
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Mitochondrial abnormalities in Alzheimer's disease.

TL;DR: Morphometric analysis showed that mitochondria are significantly reduced in Alzheimer's disease, and the relationship shown here between the site and extent of mitochondrial abnormalities and oxidative damage suggests an intimate and early association between these features in dementia.
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Activation and redistribution of c-jun N-terminal kinase/stress activated protein kinase in degenerating neurons in Alzheimer's disease.

TL;DR: Findings suggest that JNK/SAPK dysregulation, probably resulting from oxidative stress, plays an important role in the increased phosphorylation of cytoskeletal proteins found in AD.
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Role of mitochondrial dysfunction in Alzheimer's disease.

TL;DR: 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 are reviewed.