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Aβ Behavior on Neuronal Membranes: Aggregation and Toxicities

Aβ Behavior on Neuronal Membranes: Aggregation and Toxicities SAGE-Hindawi Access to Research International Journal of Alzheimer’s Disease Volume 2011, Article ID 286536, 2 pages doi:10.4061/2011/286536 Editorial Aβ Behavior on Neuronal Membranes: Aggregation and Toxicities 1 2 3 4 Katsuhiko Yanagisawa, Jacques Fantini, Avijit Chakrabartty, and Anne Eckert Research Institute, National Center for Geriatrics and Gerontology, Obu, Aichi 474-8522, Japan Centre de Recherche en Neurobiologie et Neurophysiologie de Marseille (CRN2M), Universit´edelaM´editerran´ee Aix-Marseille II et Universit´ePaulC´ezanne Aix-Marseille III, CNRS UMR 6231, INRA USC 2027, 13284 Marseille Cedex 07, France Department of Medical Biophysics, Ontario Cancer Institute, University of Toronto, TMDT 4-305, 101 College Street, Toronto, ON, Canada M5G 1L7 Neurobiology Laboratory for Brain Aging and Mental Health, Psychiatric University Clinics, University of Basel, 4025 Basel, Switzerland Correspondence should be addressed to Katsuhiko Yanagisawa, katuhiko@ncgg.go.jp Received 1 March 2011; Accepted 1 March 2011 Copyright © 2011 Katsuhiko Yanagisawa et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. A growing body of evidence suggests that the aggregation channels in the neuronal membranes, resulting in the disrup- and toxic potentials of amyloidogenic proteins, including tion of calcium homeostasis that is critical for the function amyloid β-protein (Aβ), α-synuclein, and prion protein, and survival of neurons, and the possibility of generation of radicals. In regard to the Aβ toxicities, much attention has emerge through the interaction of these proteins with been paid to the argument that the accumulation of Aβ inside neuronal and/or glial membranes. The aggregation and neurons may be the critical step. In this context, the next deposition of Aβ are the initial events of Alzheimer’s disease two papers propose a mechanism by which Aβ enters the (AD), and the toxicity of aggregated Aβ is the basis for neurons, which are followed by another two papers showing the neuronal loss in AD brains. Thus, the Aβ behavior on how the internalized Aβ acts pathologically inside neurons, neuronal membranes should be one of the critical issues to emphasizing the possibility that the mitochondria may be a be clarified for our further understanding of the pathogenesis target of intraneuronal Aβ. of AD and to develop therapeutic strategies. To accelerate A further argument for the possible interaction between studies in this field, we have invited original research articles Aβ and neuronal membranes is presented in the next four as well as review articles that will provide novel information papers. In these papers, it is presented how Aβ affects the for our special issue. properties of neuronal membranes or, conversely, how the The first three papers of this special issue describe the alteration of membrane properties affects the processing of crucial involvement of lipid rafts, which are specific mem- amyloid precursor protein (APP) leading to Aβ generation. brane microdomains on the cell surface that are rich in sph- Note that the metabolism of neuronal lipids, particularly ingolipids and cholesterol, in the production, aggregation, sphingolipids and ceramide, can be regulated in association and toxicities of Aβ. The subsequent three papers focus on with APP processing. the gangliosides, which are the major constituent of lipid The final paper of this special issue describes a fore- rafts, particularly in terms of their role in the induction of sighted aspect of science and technology of nanochemistry conformational changes of Aβ, leading to their aggregation with respect to the pathological protein aggregation, which is and emerging toxicities. likely based on the catalysts of membrane lipids, suggesting The next two articles address how Aβ causes neuronal an opportunity for developing novel nanomedicines and injury by showing the possibility of formation of amyloid nanodiagnostics for various amyloidoses. 2 International Journal of Alzheimer’s Disease We all look forward to seeing further expansion of studies in this field in the near future. Katsuhiko Yanagisawa Jacques Fantini Avijit Chakrabartty Anne Eckert MEDIATORS of INFLAMMATION The Scientific Gastroenterology Journal of World Journal Research and Practice Diabetes Research Disease Markers Hindawi Publishing Corporation Hindawi Publishing Corporation Hindawi Publishing Corporation Hindawi Publishing Corporation Hindawi Publishing Corporation http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 International Journal of Journal of Immunology Research Endocrinology Hindawi Publishing Corporation Hindawi Publishing Corporation http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 Submit your manuscripts at http://www.hindawi.com BioMed PPAR Research Research International Hindawi Publishing Corporation Hindawi Publishing Corporation http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 Journal of Obesity Evidence-Based Journal of Journal of Stem Cells Complementary and Ophthalmology International Alternative Medicine Oncology Hindawi Publishing Corporation Hindawi Publishing Corporation Hindawi Publishing Corporation Hindawi Publishing Corporation Hindawi Publishing Corporation http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 Parkinson’s Disease Computational and Behavioural Mathematical Methods AIDS Oxidative Medicine and in Medicine Research and Treatment Cellular Longevity Neurology Hindawi Publishing Corporation Hindawi Publishing Corporation Hindawi Publishing Corporation Hindawi Publishing Corporation Hindawi Publishing Corporation http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png International Journal of Alzheimer's Disease Hindawi Publishing Corporation

Aβ Behavior on Neuronal Membranes: Aggregation and Toxicities

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Publisher
Hindawi Publishing Corporation
Copyright
Copyright © 2011 Katsuhiko Yanagisawa et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
ISSN
2090-8024
DOI
10.4061/2011/286536
Publisher site
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Abstract

SAGE-Hindawi Access to Research International Journal of Alzheimer’s Disease Volume 2011, Article ID 286536, 2 pages doi:10.4061/2011/286536 Editorial Aβ Behavior on Neuronal Membranes: Aggregation and Toxicities 1 2 3 4 Katsuhiko Yanagisawa, Jacques Fantini, Avijit Chakrabartty, and Anne Eckert Research Institute, National Center for Geriatrics and Gerontology, Obu, Aichi 474-8522, Japan Centre de Recherche en Neurobiologie et Neurophysiologie de Marseille (CRN2M), Universit´edelaM´editerran´ee Aix-Marseille II et Universit´ePaulC´ezanne Aix-Marseille III, CNRS UMR 6231, INRA USC 2027, 13284 Marseille Cedex 07, France Department of Medical Biophysics, Ontario Cancer Institute, University of Toronto, TMDT 4-305, 101 College Street, Toronto, ON, Canada M5G 1L7 Neurobiology Laboratory for Brain Aging and Mental Health, Psychiatric University Clinics, University of Basel, 4025 Basel, Switzerland Correspondence should be addressed to Katsuhiko Yanagisawa, katuhiko@ncgg.go.jp Received 1 March 2011; Accepted 1 March 2011 Copyright © 2011 Katsuhiko Yanagisawa et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. A growing body of evidence suggests that the aggregation channels in the neuronal membranes, resulting in the disrup- and toxic potentials of amyloidogenic proteins, including tion of calcium homeostasis that is critical for the function amyloid β-protein (Aβ), α-synuclein, and prion protein, and survival of neurons, and the possibility of generation of radicals. In regard to the Aβ toxicities, much attention has emerge through the interaction of these proteins with been paid to the argument that the accumulation of Aβ inside neuronal and/or glial membranes. The aggregation and neurons may be the critical step. In this context, the next deposition of Aβ are the initial events of Alzheimer’s disease two papers propose a mechanism by which Aβ enters the (AD), and the toxicity of aggregated Aβ is the basis for neurons, which are followed by another two papers showing the neuronal loss in AD brains. Thus, the Aβ behavior on how the internalized Aβ acts pathologically inside neurons, neuronal membranes should be one of the critical issues to emphasizing the possibility that the mitochondria may be a be clarified for our further understanding of the pathogenesis target of intraneuronal Aβ. of AD and to develop therapeutic strategies. To accelerate A further argument for the possible interaction between studies in this field, we have invited original research articles Aβ and neuronal membranes is presented in the next four as well as review articles that will provide novel information papers. In these papers, it is presented how Aβ affects the for our special issue. properties of neuronal membranes or, conversely, how the The first three papers of this special issue describe the alteration of membrane properties affects the processing of crucial involvement of lipid rafts, which are specific mem- amyloid precursor protein (APP) leading to Aβ generation. brane microdomains on the cell surface that are rich in sph- Note that the metabolism of neuronal lipids, particularly ingolipids and cholesterol, in the production, aggregation, sphingolipids and ceramide, can be regulated in association and toxicities of Aβ. The subsequent three papers focus on with APP processing. the gangliosides, which are the major constituent of lipid The final paper of this special issue describes a fore- rafts, particularly in terms of their role in the induction of sighted aspect of science and technology of nanochemistry conformational changes of Aβ, leading to their aggregation with respect to the pathological protein aggregation, which is and emerging toxicities. likely based on the catalysts of membrane lipids, suggesting The next two articles address how Aβ causes neuronal an opportunity for developing novel nanomedicines and injury by showing the possibility of formation of amyloid nanodiagnostics for various amyloidoses. 2 International Journal of Alzheimer’s Disease We all look forward to seeing further expansion of studies in this field in the near future. Katsuhiko Yanagisawa Jacques Fantini Avijit Chakrabartty Anne Eckert MEDIATORS of INFLAMMATION The Scientific Gastroenterology Journal of World Journal Research and Practice Diabetes Research Disease Markers Hindawi Publishing Corporation Hindawi Publishing Corporation Hindawi Publishing Corporation Hindawi Publishing Corporation Hindawi Publishing Corporation http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 International Journal of Journal of Immunology Research Endocrinology Hindawi Publishing Corporation Hindawi Publishing Corporation http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 Submit your manuscripts at http://www.hindawi.com BioMed PPAR Research Research International Hindawi Publishing Corporation Hindawi Publishing Corporation http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 Journal of Obesity Evidence-Based Journal of Journal of Stem Cells Complementary and Ophthalmology International Alternative Medicine Oncology Hindawi Publishing Corporation Hindawi Publishing Corporation Hindawi Publishing Corporation Hindawi Publishing Corporation Hindawi Publishing Corporation http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 Parkinson’s Disease Computational and Behavioural Mathematical Methods AIDS Oxidative Medicine and in Medicine Research and Treatment Cellular Longevity Neurology Hindawi Publishing Corporation Hindawi Publishing Corporation Hindawi Publishing Corporation Hindawi Publishing Corporation Hindawi Publishing Corporation http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014 http://www.hindawi.com Volume 2014

Journal

International Journal of Alzheimer's DiseaseHindawi Publishing Corporation

Published: Jul 6, 2011

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