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  • 1
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    Age-associated inclusions in normal and transgenic mouse brain (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-03-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jucker, M -- Walker, L C -- Martin, L J -- Kitt, C A -- Kleinman, H K -- Ingram, D K -- Price, D L -- New York, N.Y. -- Science. 1992 Mar 13;255(5050):1443-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1542796" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*metabolism ; Amyloid beta-Peptides/*metabolism ; Animals ; Brain/*metabolism ; Female ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Peripherally applied Abeta-containing inoculates induce cerebral beta-amyloidosis (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-10-23
    Description: The intracerebral injection of beta-amyloid-containing brain extracts can induce cerebral beta-amyloidosis and associated pathologies in susceptible hosts. We found that intraperitoneal inoculation with beta-amyloid-rich extracts induced beta-amyloidosis in the brains of beta-amyloid precursor protein transgenic mice after prolonged incubation times.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3233904/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3233904/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eisele, Yvonne S -- Obermuller, Ulrike -- Heilbronner, Gotz -- Baumann, Frank -- Kaeser, Stephan A -- Wolburg, Hartwig -- Walker, Lary C -- Staufenbiel, Matthias -- Heikenwalder, Mathias -- Jucker, Mathias -- P51 RR000165/RR/NCRR NIH HHS/ -- P51 RR000165-51/RR/NCRR NIH HHS/ -- RR-00165/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2010 Nov 12;330(6006):980-2. doi: 10.1126/science.1194516. Epub 2010 Oct 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular Neurology, Hertie-Institute for Clinical Brain Research, University of Tubingen, D-72076 Tubingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20966215" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/metabolism/pathology ; Amyloid beta-Peptides/administration & dosage/*chemistry/metabolism ; Animals ; Brain/blood supply/*pathology ; Brain Chemistry ; Cerebral Amyloid Angiopathy/metabolism/pathology ; Female ; Injections, Intraperitoneal ; Mice ; Mice, Transgenic ; Plaque, Amyloid/pathology ; Prions/chemistry/metabolism ; Protein Folding ; Time Factors
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Exogenous induction of cerebral beta-amyloidogenesis is governed by agent and host (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-09-23
    Description: Protein aggregation is an established pathogenic mechanism in Alzheimer's disease, but little is known about the initiation of this process in vivo. Intracerebral injection of dilute, amyloid-beta (Abeta)-containing brain extracts from humans with Alzheimer's disease or beta-amyloid precursor protein (APP) transgenic mice induced cerebral beta-amyloidosis and associated pathology in APP transgenic mice in a time- and concentration-dependent manner. The seeding activity of brain extracts was reduced or abolished by Abeta immunodepletion, protein denaturation, or by Abeta immunization of the host. The phenotype of the exogenously induced amyloidosis depended on both the host and the source of the agent, suggesting the existence of polymorphic Abeta strains with varying biological activities reminiscent of prion strains.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meyer-Luehmann, Melanie -- Coomaraswamy, Janaky -- Bolmont, Tristan -- Kaeser, Stephan -- Schaefer, Claudia -- Kilger, Ellen -- Neuenschwander, Anton -- Abramowski, Dorothee -- Frey, Peter -- Jaton, Anneliese L -- Vigouret, Jean-Marie -- Paganetti, Paolo -- Walsh, Dominic M -- Mathews, Paul M -- Ghiso, Jorge -- Staufenbiel, Matthias -- Walker, Lary C -- Jucker, Mathias -- NS45357/NS/NINDS NIH HHS/ -- RR-00165/RR/NCRR NIH HHS/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2006 Sep 22;313(5794):1781-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular Neurology, Hertie-Institute for Clinical Brain Research, University of Tubingen, D-72076 Tubingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16990547" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Aged, 80 and over ; Aging ; Alzheimer Disease/metabolism ; Amyloid beta-Peptides/*administration & dosage/*analysis/chemistry/pharmacology ; Amyloid beta-Protein Precursor/*administration & dosage/pharmacology ; Amyloidosis/*metabolism/pathology ; Animals ; Brain/pathology ; Brain Chemistry ; Brain Diseases/*metabolism/pathology ; Female ; Hippocampus/*chemistry/pathology ; Humans ; Male ; Mice ; Mice, Transgenic ; Protein Denaturation ; Time Factors ; Tissue Extracts
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 4
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    Self-propagation of pathogenic protein aggregates in neurodegenerative diseases (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-09-06
    Description: For several decades scientists have speculated that the key to understanding age-related neurodegenerative disorders may be found in the unusual biology of the prion diseases. Recently, owing largely to the advent of new disease models, this hypothesis has gained experimental momentum. In a remarkable variety of diseases, specific proteins have been found to misfold and aggregate into seeds that structurally corrupt like proteins, causing them to aggregate and form pathogenic assemblies ranging from small oligomers to large masses of amyloid. Proteinaceous seeds can therefore serve as self-propagating agents for the instigation and progression of disease. Alzheimer's disease and other cerebral proteopathies seem to arise from the de novo misfolding and sustained corruption of endogenous proteins, whereas prion diseases can also be infectious in origin. However, the outcome in all cases is the functional compromise of the nervous system, because the aggregated proteins gain a toxic function and/or lose their normal function. As a unifying pathogenic principle, the prion paradigm suggests broadly relevant therapeutic directions for a large class of currently intractable diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3963807/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3963807/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jucker, Mathias -- Walker, Lary C -- P51 OD011132/OD/NIH HHS/ -- P51 RR000165/RR/NCRR NIH HHS/ -- P51OD11132/OD/NIH HHS/ -- P51RR165/RR/NCRR NIH HHS/ -- R21 AG040589/AG/NIA NIH HHS/ -- R21AG040589/AG/NIA NIH HHS/ -- England -- Nature. 2013 Sep 5;501(7465):45-51. doi: 10.1038/nature12481.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, D-72076 Tubingen, Germany. mathias.jucker@uni-tuebingen.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24005412" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/metabolism/pathology ; Amyloid/chemistry/*metabolism ; Animals ; Humans ; Neurodegenerative Diseases/drug therapy/*metabolism/*pathology ; Prion Diseases/drug therapy/metabolism/pathology ; Prions/chemistry/classification/*metabolism ; alpha-Synuclein/chemistry/metabolism ; tau Proteins/chemistry/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 5
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    Neurodegeneration: Amyloid-beta pathology induced in humans (2015)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2015-09-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jucker, Mathias -- Walker, Lary C -- England -- Nature. 2015 Sep 10;525(7568):193-4. doi: 10.1038/525193a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hertie Institute for Clinical Brain Research, University of Tubingen, and at the German Center for Neurodegenerative Diseases (DZNE), D-72076 Tubingen, Germany. ; Yerkes National Primate Research Center and Department of Neurology, Emory University, Atlanta, Georgia 30322, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26354478" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*etiology ; Amyloid beta-Peptides/*metabolism ; Cerebral Amyloid Angiopathy/*etiology ; Creutzfeldt-Jakob Syndrome/*etiology ; *Drug Contamination ; Human Growth Hormone/*administration & dosage ; Humans ; *Iatrogenic Disease
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 6
    Electronic Resource
    Electronic Resource
    The Age of Biosenescence and the Incidence of Cerebral β-Amyloidosis in Aged Captive Rhesus Monkeys (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 695 (1993), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Notes: Autopsy surveillance of 186 rhesus monkeys aged 20 to 36 years revealed that development of major geriatric diseases such as emphysema, coronary sclerosis, and cancer increased rapidly after the age of 25 years, and nearly 70% of the monkeys in each cohort group died by 30 years. According to our 12-year longitudinal survey, the age of biosenescence in captive rhesus monkeys begins around 25 years and the maximum longevity is 36 years. The incidence of cerebral β-amyloidosis associated with plaque formation and cerebral angiopathy was observed in 51 brains of rhesus monkeys aged 25 to 36 years. Lesions were found in 31 of 51 aged brains (60%) and 6 monkeys over 34 years of age were all severely affected. Despite the size of the plaque, nearly all of them showed immunopositive β-amyloid. Cerebral angiopathy coexisted in 10 of 31 plaque-positive brains. The basal prefrontal gyms was the most common site and contained the highest density of plaques, followed by the amygdala region. The amyloid in the liver, spleen, adrenal and pancreatic islets in visceral amyloidosis showed no positivity to the β-amyloid demonstrated in the brain. As in aged human brains, the incidence of age-dependent cerebral β-amyloidosis in captive rhesus monkeys showed great individual variation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1993.tb23058.x
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    Paper (German National Licenses)
    Fulltext
  • 7
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    Induction of cerebral  -amyloidosis: Intracerebral versus systemic A  inoculation (2009)
    National Academy of Sciences
    Details
    Publication Date: 2009-07-21
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 8
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    Movement of Nutrients in Coastal Bermudagrass 1 (1962)
    Wiley
    Details
    Publication Date: 1962-09-01
    Print ISSN: 0002-1962
    Electronic ISSN: 1435-0645
    Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition
    Published by Wiley
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  • 9
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    Thermodynamic Properties of Aluminum Hydride (1967)
    American Institute of Physics
    Details
    Publication Date: 1967-10-15
    Print ISSN: 0021-9606
    Electronic ISSN: 1089-7690
    Topics: Chemistry and Pharmacology , Physics
    Published by American Institute of Physics
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  • 10
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    Erratum: Circularly Polarized X Rays as a Probe of Noncollinear Magnetic Order in Multiferroic TbMnO_{3} [Phys. Rev. Lett. 102, 237205 (2009)] (2011)
    American Physical Society (APS)
    Details
    Publication Date: 2011-06-11
    Description: Author(s): F. Fabrizi, H. C. Walker, L. Paolasini, F. de Bergevin, A. T. Boothroyd, D. Prabhakaran, and D. F. McMorrow [Phys. Rev. Lett. 106, 239902] Published Fri Jun 10, 2011
    Keywords: Errata
    Print ISSN: 0031-9007
    Electronic ISSN: 1079-7114
    Topics: Physics
    Published by American Physical Society (APS)
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