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Amyloid beta peptides induce mitochondrial dysfunction and oxidative stress in astrocytes and death of neurons through activation of NADPH oxidase.
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The article was published on 2004-01-01 and is currently open access. It has received 453 citations till now. The article focuses on the topics: Amyloid beta & NADPH oxidase.read more
Citations
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Journal ArticleDOI
Neurovascular regulation in the normal brain and in Alzheimer's disease.
TL;DR: The emerging view is that cerebroVascular dysregulation is a feature not only of cerebrovascular pathologies, such as stroke, but also of neurodegenerative conditions, suchas Alzheimer's disease.
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Expression of a noncoding RNA is elevated in Alzheimer's disease and drives rapid feed-forward regulation of β-secretase
Mohammad Ali Faghihi,Mohammad Ali Faghihi,Farzaneh Modarresi,Ahmad M. Khalil,Douglas E. Wood,Barbara G. Sahagan,Todd E. Morgan,Caleb E. Finch,Georges St. Laurent,Georges St. Laurent,Paul J. Kenny,Claes Wahlestedt +11 more
TL;DR: It is reported that a long noncoding RNA is directly implicated in the increased abundance of Aβ 1–42 in Alzheimer's disease.
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NAD+/NADH and NADP+/NADPH in Cellular Functions and Cell Death: Regulation and Biological Consequences
TL;DR: Future investigation into the metabolism and biological functions of NAD and NADP may expose fundamental properties of life, and suggest new strategies for treating diseases and slowing the aging process.
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Molecular Docking and Structure-Based Drug Design Strategies
TL;DR: The purpose of this review is to examine current molecular docking strategies used in drug discovery and medicinal chemistry, exploring the advances in the field and the role played by the integration of structure- and ligand-based methods.
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Inflammation in Alzheimer Disease—A Brief Review of the Basic Science and Clinical Literature
Tony Wyss-Coray,Joseph Rogers +1 more
TL;DR: Biochemical and neuropathological studies of brains from individuals with Alzheimer disease provide clear evidence for an activation of inflammatory pathways, and long-term use of anti-inflammatory drugs is linked with reduced risk to develop the disease.
References
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Free Radicals in the Physiological Control of Cell Function
TL;DR: There is growing evidence that aging involves, in addition, progressive changes in free radical-mediated regulatory processes that result in altered gene expression.
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Correlation Between Elevated Levels of Amyloid β-Peptide in the Brain and Cognitive Decline
Jan Näslund,Vahram Haroutunian,Richard C. Mohs,Kenneth L. Davis,Peter Davies,Paul Greengard,Joseph D. Buxbaum +6 more
TL;DR: An important role for Abeta in mediating initial pathogenic events in AD dementia is supported and treatment strategies targeting the formation, accumulation, or cytotoxic effects of Abeta should be pursued.
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Mitochondrial abnormalities in Alzheimer's disease.
Keisuke Hirai,Gjumrakch Aliev,Akihiko Nunomura,Akihiko Nunomura,Hisashi Fujioka,Robert L. Russell,Craig S. Atwood,Anne B. Johnson,Yvonne Kress,Harry V. Vinters,Massimo Tabaton,Shun Shimohama,Adam D. Cash,Sandra L. Siedlak,Peggy L.R. Harris,Paul K. Jones,Robert B. Petersen,George Perry,Mark A. Smith +18 more
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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Mitochondria and calcium: from cell signalling to cell death
TL;DR: Accumulation of Ca2+ into mitochondria regulates mitochondrial metabolism and causes a transient depolarisation of mitochondrial membrane potential, and alteration of spatiotemporal characteristics of cellular [Ca2+]c signalling and downregulates mitochondrial metabolism.
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Amyloid β protein forms ion channels: implications for Alzheimer’s disease pathophysiology
TL;DR: AβP channels may provide a direct pathway for calcium‐dependent AβP toxicity in AD by allowing calcium uptake and induces neuritic abnormality in a dose‐ and time‐dependent fashion.