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| Home > Publications Database > Acute targeting of pre-amyloid seeds in transgenic mice reduces Alzheimer-like pathology later in life. > print |
| 001 | 154283 | ||
| 005 | 20230915094032.0 | ||
| 024 | 7 | _ | |a 10.1038/s41593-020-00737-w |2 doi |
| 024 | 7 | _ | |a pmid:33199898 |2 pmid |
| 024 | 7 | _ | |a pmc:PMC7783656 |2 pmc |
| 024 | 7 | _ | |a 1097-6256 |2 ISSN |
| 024 | 7 | _ | |a 1546-1726 |2 ISSN |
| 024 | 7 | _ | |a altmetric:94397111 |2 altmetric |
| 037 | _ | _ | |a DZNE-2021-00137 |
| 041 | _ | _ | |a English |
| 082 | _ | _ | |a 610 |
| 100 | 1 | _ | |a Uhlmann, Ruth E |0 P:(DE-2719)9001482 |b 0 |e First author |u dzne |
| 245 | _ | _ | |a Acute targeting of pre-amyloid seeds in transgenic mice reduces Alzheimer-like pathology later in life. |
| 260 | _ | _ | |a New York, NY |c 2020 |b Nature America |
| 336 | 7 | _ | |a article |2 DRIVER |
| 336 | 7 | _ | |a Output Types/Journal article |2 DataCite |
| 336 | 7 | _ | |a Journal Article |b journal |m journal |0 PUB:(DE-HGF)16 |s 1618915032_3883 |2 PUB:(DE-HGF) |
| 336 | 7 | _ | |a ARTICLE |2 BibTeX |
| 336 | 7 | _ | |a JOURNAL_ARTICLE |2 ORCID |
| 336 | 7 | _ | |a Journal Article |0 0 |2 EndNote |
| 500 | _ | _ | |a ISSN 1546-1726 not unique: **3 hits**. |
| 520 | _ | _ | |a Amyloid-β (Aβ) deposits are a relatively late consequence of Aβ aggregation in Alzheimer's disease. When pathogenic Aβ seeds begin to form, propagate and spread is not known, nor are they biochemically defined. We tested various antibodies for their ability to neutralize Aβ seeds before Aβ deposition becomes detectable in Aβ precursor protein-transgenic mice. We also characterized the different antibody recognition profiles using immunoprecipitation of size-fractionated, native, mouse and human brain-derived Aβ assemblies. At least one antibody, aducanumab, after acute administration at the pre-amyloid stage, led to a significant reduction of Aβ deposition and downstream pathologies 6 months later. This demonstrates that therapeutically targetable pathogenic Aβ seeds already exist during the lag phase of protein aggregation in the brain. Thus, the preclinical phase of Alzheimer's disease-currently defined as Aβ deposition without clinical symptoms-may be a relatively late manifestation of a much earlier pathogenic seed formation and propagation that currently escapes detection in vivo. |
| 536 | _ | _ | |a 342 - Disease Mechanisms and Model Systems (POF3-342) |0 G:(DE-HGF)POF3-342 |c POF3-342 |f POF III |x 0 |
| 588 | _ | _ | |a Dataset connected to CrossRef, PubMed, , Journals: pub.dzne.de |
| 650 | _ | 7 | |a Amyloid beta-Peptides |2 NLM Chemicals |
| 650 | _ | 7 | |a Amyloid beta-Protein Precursor |2 NLM Chemicals |
| 650 | _ | 7 | |a Antibodies, Blocking |2 NLM Chemicals |
| 650 | _ | 7 | |a Antibodies, Monoclonal, Humanized |2 NLM Chemicals |
| 650 | _ | 7 | |a Neurofilament Proteins |2 NLM Chemicals |
| 650 | _ | 7 | |a Tissue Extracts |2 NLM Chemicals |
| 650 | _ | 7 | |a aducanumab |0 105J35OE21 |2 NLM Chemicals |
| 650 | _ | 2 | |a Aged |2 MeSH |
| 650 | _ | 2 | |a Aged, 80 and over |2 MeSH |
| 650 | _ | 2 | |a Alzheimer Disease: metabolism |2 MeSH |
| 650 | _ | 2 | |a Alzheimer Disease: pathology |2 MeSH |
| 650 | _ | 2 | |a Amyloid beta-Peptides: metabolism |2 MeSH |
| 650 | _ | 2 | |a Amyloid beta-Protein Precursor: antagonists & inhibitors |2 MeSH |
| 650 | _ | 2 | |a Animals |2 MeSH |
| 650 | _ | 2 | |a Antibodies, Blocking: pharmacology |2 MeSH |
| 650 | _ | 2 | |a Antibodies, Monoclonal, Humanized: pharmacokinetics |2 MeSH |
| 650 | _ | 2 | |a Antibodies, Monoclonal, Humanized: pharmacology |2 MeSH |
| 650 | _ | 2 | |a Brain Chemistry |2 MeSH |
| 650 | _ | 2 | |a Humans |2 MeSH |
| 650 | _ | 2 | |a Male |2 MeSH |
| 650 | _ | 2 | |a Mice |2 MeSH |
| 650 | _ | 2 | |a Mice, Inbred C57BL |2 MeSH |
| 650 | _ | 2 | |a Mice, Transgenic |2 MeSH |
| 650 | _ | 2 | |a Middle Aged |2 MeSH |
| 650 | _ | 2 | |a Neurofilament Proteins: cerebrospinal fluid |2 MeSH |
| 650 | _ | 2 | |a Plaque, Amyloid: pathology |2 MeSH |
| 650 | _ | 2 | |a Tissue Extracts: pharmacology |2 MeSH |
| 700 | 1 | _ | |a Rother, Christine |0 P:(DE-2719)9001483 |b 1 |u dzne |
| 700 | 1 | _ | |a Rasmussen, Jay |0 P:(DE-2719)2811173 |b 2 |
| 700 | 1 | _ | |a Schelle, Juliane |0 P:(DE-2719)2811018 |b 3 |
| 700 | 1 | _ | |a Bergmann, Carina |0 P:(DE-2719)9001484 |b 4 |u dzne |
| 700 | 1 | _ | |a Ullrich Gavilanes, Emily M |0 P:(DE-2719)9001485 |b 5 |u dzne |
| 700 | 1 | _ | |a Fritschi, Sarah |0 P:(DE-2719)2451359 |b 6 |
| 700 | 1 | _ | |a Buehler, Anika |0 P:(DE-2719)2813030 |b 7 |
| 700 | 1 | _ | |a Baumann, Frank |0 P:(DE-2719)9000018 |b 8 |
| 700 | 1 | _ | |a Skodras, Angelos |0 P:(DE-2719)2810430 |b 9 |
| 700 | 1 | _ | |a Al-Shaana, Rawaa |0 P:(DE-2719)9001466 |b 10 |u dzne |
| 700 | 1 | _ | |a Beschorner, Natalie |0 P:(DE-2719)9001120 |b 11 |
| 700 | 1 | _ | |a Ye, Lan |0 P:(DE-2719)2811684 |b 12 |
| 700 | 1 | _ | |a Kaeser, Stephan A |0 P:(DE-2719)9000387 |b 13 |
| 700 | 1 | _ | |a Obermüller, Ulrike |0 P:(DE-2719)2814201 |b 14 |
| 700 | 1 | _ | |a Christensen, Søren |b 15 |
| 700 | 1 | _ | |a Kartberg, Fredrik |b 16 |
| 700 | 1 | _ | |a Stavenhagen, Jeffrey B |b 17 |
| 700 | 1 | _ | |a Rahfeld, Jens-Ulrich |b 18 |
| 700 | 1 | _ | |a Cynis, Holger |0 0000-0001-6655-7539 |b 19 |
| 700 | 1 | _ | |a Qian, Fang |b 20 |
| 700 | 1 | _ | |a Weinreb, Paul H |0 0000-0002-0802-0052 |b 21 |
| 700 | 1 | _ | |a Bussiere, Thierry |0 0000-0002-6818-4876 |b 22 |
| 700 | 1 | _ | |a Walker, Lary C |0 P:(DE-HGF)0 |b 23 |
| 700 | 1 | _ | |a Staufenbiel, Matthias |0 P:(DE-HGF)0 |b 24 |
| 700 | 1 | _ | |a Jucker, Mathias |0 P:(DE-2719)2000010 |b 25 |e Last author |
| 773 | _ | _ | |a 10.1038/s41593-020-00737-w |g Vol. 23, no. 12, p. 1580 - 1588 |0 PERI:(DE-600)1494955-6 |n 12 |p 1580 - 1588 |t Nature neuroscience |v 23 |y 2020 |x 1546-1726 |
| 856 | 4 | _ | |u https://pubmed.ncbi.nlm.nih.gov/33199898/ |
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