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Hardcover. Condition: Good. HARDCOVER Good - Bumped and creased book with tears to the extremities, but not affecting the text block, may have remainder mark or previous owner's name - GOOD Standard-sized.
Language: English
Published by Birkhauser Boston Inc, US, 2012
ISBN 10: 1461581516 ISBN 13: 9781461581512
Seller: Rarewaves.com USA, London, LONDO, United Kingdom
Paperback. Condition: New. Softcover reprint of the original 1st ed. 1994.
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Seller: Ria Christie Collections, Uxbridge, United Kingdom
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Seller: Kennys Bookshop and Art Galleries Ltd., Galway, GY, Ireland
Condition: New. 2012. Softcover reprint of the original 1st ed. 1994. paperback. . . . . .
Condition: New. pp. 508.
Condition: New. pp. 530.
Condition: New. 2012. Softcover reprint of the original 1st ed. 1994. paperback. . . . . . Books ship from the US and Ireland.
Seller: Revaluation Books, Exeter, United Kingdom
Paperback. Condition: Brand New. reprint edition. 509 pages. 9.00x6.00x1.25 inches. In Stock.
Taschenbuch. Condition: Neu. Alzheimer Disease | Therapeutic Strategies | Ezio Giacobini (u. a.) | Taschenbuch | xvi | Englisch | 2012 | Birkhäuser | EAN 9781461581512 | Verantwortliche Person für die EU: Springer Basel AG in Springer Science + Business Media, Heidelberger Platz 3, 14197 Berlin, juergen[dot]hartmann[at]springer[dot]com | Anbieter: preigu.
Language: English
Published by Birkhäuser, Birkhäuser, 2012
ISBN 10: 1461581516 ISBN 13: 9781461581512
Seller: AHA-BUCH GmbH, Einbeck, Germany
Taschenbuch. Condition: Neu. Druck auf Anfrage Neuware - Printed after ordering - Since the apoE4 allele is a risk factor or susceptibility gene in late-onset familial and sporadic AD, the mechanism of disease expression may involve metabolic effects that are isoform specific. Isoform-specific interactions of apoE therefore become critical in the mechanism of AD pathogenesis. Detailed characterization of the binding of the apoE isoforms with proteins and peptides relevant to the pathology of the disease may be critical in understanding disease pathogenesis. These critical isoform-specific interactions of apoE may involve interactions with proteins and pep tides in the defining neuropathologic lesions of the disease, the neurofibrillary tangle and senile plaque. Other possible critical isoform-specific interactions include the mechanism of internalization, intracellular trafficking, and subsequent metabolism. In addition, differential post-translational modifications of apoE isoforms may determine differences in metabolism contributing to the pathogenesis of the disease. Oxidation of apoE may confer several isoform-specific, biochemically distinct properties. Since {3A peptide binds apoE in the lipoprotein binding domain of the protein and not in the receptor-binding domain, apoE could target bound {3A4 peptide to neurons via the LRP receptor. Internalization of the apoEI {3A peptide complex into the cell, by the same route as the apoE-containing lipoproteins, would result in incorporation into primary lysosomes and pH dependent dissociation. The demonstration of apoE in the cytoplasm of neurons, with isoform-specific interactions of apoE with the microtubule-binding protein tau demonstrated in vitro, suggest additional, testable hypotheses of disease pathogenesis.
Seller: Mispah books, Redhill, SURRE, United Kingdom
Paperback. Condition: Like New. Like New. book.
Seller: Mispah books, Redhill, SURRE, United Kingdom
Paperback. Condition: Like New. Like New. book.
Language: English
Published by Birkhauser Boston Inc, US, 2012
ISBN 10: 1461581516 ISBN 13: 9781461581512
Seller: Rarewaves.com UK, London, United Kingdom
Paperback. Condition: New. Softcover reprint of the original 1st ed. 1994.
Condition: Sehr gut. Zustand: Sehr gut | Seiten: 528 | Sprache: Englisch | Produktart: Bücher | Since the apoE4 allele is a risk factor or susceptibility gene in late-onset familial and sporadic AD, the mechanism of disease expression may involve metabolic effects that are isoform specific. Isoform-specific interactions of apoE therefore become critical in the mechanism of AD pathogenesis. Detailed characterization of the binding of the apoE isoforms with proteins and peptides relevant to the pathology of the disease may be critical in understanding disease pathogenesis. These critical isoform-specific interactions of apoE may involve interactions with proteins and pep tides in the defining neuropathologic lesions of the disease, the neurofibrillary tangle and senile plaque. Other possible critical isoform-specific interactions include the mechanism of internalization, intracellular trafficking, and subsequent metabolism. In addition, differential post-translational modifications of apoE isoforms may determine differences in metabolism contributing to the pathogenesis of the disease. Oxidation of apoE may confer several isoform-specific, biochemically distinct properties. Since {3A peptide binds apoE in the lipoprotein binding domain of the protein and not in the receptor-binding domain, apoE could target bound {3A4 peptide to neurons via the LRP receptor. Internalization of the apoEI {3A peptide complex into the cell, by the same route as the apoE-containing lipoproteins, would result in incorporation into primary lysosomes and pH dependent dissociation. The demonstration of apoE in the cytoplasm of neurons, with isoform-specific interactions of apoE with the microtubule-binding protein tau demonstrated in vitro, suggest additional, testable hypotheses of disease pathogenesis.
Condition: Used. pp. 632.
Seller: GreatBookPricesUK, Woodford Green, United Kingdom
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Seller: GreatBookPrices, Columbia, MD, U.S.A.
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Seller: Brook Bookstore On Demand, Napoli, NA, Italy
Condition: new. Questo è un articolo print on demand.
Language: English
Published by Birkhäuser Boston Mai 2012, 2012
ISBN 10: 1461581516 ISBN 13: 9781461581512
Seller: BuchWeltWeit Ludwig Meier e.K., Bergisch Gladbach, Germany
Taschenbuch. Condition: Neu. This item is printed on demand - it takes 3-4 days longer - Neuware -Since the apoE4 allele is a risk factor or susceptibility gene in late-onset familial and sporadic AD, the mechanism of disease expression may involve metabolic effects that are isoform specific. Isoform-specific interactions of apoE therefore become critical in the mechanism of AD pathogenesis. Detailed characterization of the binding of the apoE isoforms with proteins and peptides relevant to the pathology of the disease may be critical in understanding disease pathogenesis. These critical isoform-specific interactions of apoE may involve interactions with proteins and pep tides in the defining neuropathologic lesions of the disease, the neurofibrillary tangle and senile plaque. Other possible critical isoform-specific interactions include the mechanism of internalization, intracellular trafficking, and subsequent metabolism. In addition, differential post-translational modifications of apoE isoforms may determine differences in metabolism contributing to the pathogenesis of the disease. Oxidation of apoE may confer several isoform-specific, biochemically distinct properties. Since {3A peptide binds apoE in the lipoprotein binding domain of the protein and not in the receptor-binding domain, apoE could target bound {3A4 peptide to neurons via the LRP receptor. Internalization of the apoEI {3A peptide complex into the cell, by the same route as the apoE-containing lipoproteins, would result in incorporation into primary lysosomes and pH dependent dissociation. The demonstration of apoE in the cytoplasm of neurons, with isoform-specific interactions of apoE with the microtubule-binding protein tau demonstrated in vitro, suggest additional, testable hypotheses of disease pathogenesis. 528 pp. Englisch.
Seller: Majestic Books, Hounslow, United Kingdom
Condition: New. Print on Demand pp. 508 49:B&W 6.14 x 9.21 in or 234 x 156 mm (Royal 8vo) Perfect Bound on White w/Gloss Lam.
Seller: Biblios, Frankfurt am main, HESSE, Germany
Condition: New. PRINT ON DEMAND pp. 508.
Seller: moluna, Greven, Germany
Condition: New. Dieser Artikel ist ein Print on Demand Artikel und wird nach Ihrer Bestellung fuer Sie gedruckt. Since the apoE4 allele is a risk factor or susceptibility gene in late-onset familial and sporadic AD, the mechanism of disease expression may involve metabolic effects that are isoform specific. Isoform-specific interactions of apoE therefore become critic.
Seller: Majestic Books, Hounslow, United Kingdom
Condition: New. Print on Demand pp. 530.
Seller: moluna, Greven, Germany
Condition: New. Dieser Artikel ist ein Print on Demand Artikel und wird nach Ihrer Bestellung fuer Sie gedruckt. Springer Book Archives.
Seller: Biblios, Frankfurt am main, HESSE, Germany
Condition: New. PRINT ON DEMAND pp. 530.