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| Home > Publications Database > The Tau/A152T mutation, a risk factor for frontotemporal-spectrum disorders, leads to NR2B receptor-mediated excitotoxicity. > print |
| Home > Publications Database > The Tau/A152T mutation, a risk factor for frontotemporal-spectrum disorders, leads to NR2B receptor-mediated excitotoxicity. > print |
| 001 | 138485 | ||
| 005 | 20250325124833.0 | ||
| 024 | 7 | _ | |a 10.15252/embr.201541439 |2 doi |
| 024 | 7 | _ | |a pmid:26931569 |2 pmid |
| 024 | 7 | _ | |a pmc:PMC4818782 |2 pmc |
| 024 | 7 | _ | |a 1469-221X |2 ISSN |
| 024 | 7 | _ | |a 1469-3178 |2 ISSN |
| 024 | 7 | _ | |a altmetric:6125435 |2 altmetric |
| 037 | _ | _ | |a DZNE-2020-04807 |
| 041 | _ | _ | |a English |
| 082 | _ | _ | |a 570 |
| 100 | 1 | _ | |a Decker, Jochen Martin |0 P:(DE-2719)2810343 |b 0 |e First author |u dzne |
| 245 | _ | _ | |a The Tau/A152T mutation, a risk factor for frontotemporal-spectrum disorders, leads to NR2B receptor-mediated excitotoxicity. |
| 260 | _ | _ | |a Hoboken, NJ [u.a.] |c 2016 |b Wiley |
| 264 | _ | 1 | |3 online |2 Crossref |b EMBO |c 2016-03-01 |
| 264 | _ | 1 | |3 print |2 Crossref |b EMBO |c 2016-04-01 |
| 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 1742903271_32038 |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 |
| 520 | _ | _ | |a We report on a novel transgenic mouse model expressing human full-length Tau with the Tau mutation A152T (hTau(AT)), a risk factor for FTD-spectrum disorders including PSP and CBD Brain neurons reveal pathological Tau conformation, hyperphosphorylation, mis-sorting, aggregation, neuronal degeneration, and progressive loss, most prominently in area CA3 of the hippocampus. The mossy fiber pathway shows enhanced basal synaptic transmission without changes in short- or long-term plasticity. In organotypic hippocampal slices, extracellular glutamate increases early above control levels, followed by a rise in neurotoxicity. These changes are normalized by inhibiting neurotransmitter release or by blocking voltage-gated sodium channels. CA3 neurons show elevated intracellular calcium during rest and after activity induction which is sensitive to NR2B antagonizing drugs, demonstrating a pivotal role of extrasynaptic NMDA receptors. Slices show pronounced epileptiform activity and axonal sprouting of mossy fibers. Excitotoxic neuronal death is ameliorated by ceftriaxone, which stimulates astrocytic glutamate uptake via the transporter EAAT2/GLT1. In summary, hTau(AT) causes excitotoxicity mediated by NR2B-containing NMDA receptors due to enhanced extracellular glutamate. |
| 536 | _ | _ | |a 342 - Disease Mechanisms and Model Systems (POF3-342) |0 G:(DE-HGF)POF3-342 |c POF3-342 |f POF III |x 0 |
| 536 | _ | _ | |a 341 - Molecular Signaling (POF3-341) |0 G:(DE-HGF)POF3-341 |c POF3-341 |f POF III |x 1 |
| 542 | _ | _ | |i 2016-03-01 |2 Crossref |u http://onlinelibrary.wiley.com/termsAndConditions#vor |
| 542 | _ | _ | |i 2016-03-01 |2 Crossref |u http://doi.wiley.com/10.1002/tdm_license_1.1 |
| 588 | _ | _ | |a Dataset connected to CrossRef, PubMed, |
| 650 | _ | 7 | |a Culture Media |2 NLM Chemicals |
| 650 | _ | 7 | |a NR2B NMDA receptor |2 NLM Chemicals |
| 650 | _ | 7 | |a Receptors, N-Methyl-D-Aspartate |2 NLM Chemicals |
| 650 | _ | 7 | |a tau Proteins |2 NLM Chemicals |
| 650 | _ | 7 | |a Glutamic Acid |0 3KX376GY7L |2 NLM Chemicals |
| 650 | _ | 7 | |a Calcium |0 SY7Q814VUP |2 NLM Chemicals |
| 650 | _ | 2 | |a Animals |2 MeSH |
| 650 | _ | 2 | |a CA3 Region, Hippocampal: metabolism |2 MeSH |
| 650 | _ | 2 | |a CA3 Region, Hippocampal: pathology |2 MeSH |
| 650 | _ | 2 | |a Calcium: metabolism |2 MeSH |
| 650 | _ | 2 | |a Culture Media: chemistry |2 MeSH |
| 650 | _ | 2 | |a Disease Models, Animal |2 MeSH |
| 650 | _ | 2 | |a Frontotemporal Dementia: physiopathology |2 MeSH |
| 650 | _ | 2 | |a Glutamic Acid: analysis |2 MeSH |
| 650 | _ | 2 | |a Humans |2 MeSH |
| 650 | _ | 2 | |a Mice |2 MeSH |
| 650 | _ | 2 | |a Mice, Transgenic |2 MeSH |
| 650 | _ | 2 | |a Mutation |2 MeSH |
| 650 | _ | 2 | |a Neuronal Plasticity |2 MeSH |
| 650 | _ | 2 | |a Neurons: chemistry |2 MeSH |
| 650 | _ | 2 | |a Neurons: metabolism |2 MeSH |
| 650 | _ | 2 | |a Neurons: pathology |2 MeSH |
| 650 | _ | 2 | |a Organ Culture Techniques |2 MeSH |
| 650 | _ | 2 | |a Receptors, N-Methyl-D-Aspartate: metabolism |2 MeSH |
| 650 | _ | 2 | |a Synaptic Transmission |2 MeSH |
| 650 | _ | 2 | |a tau Proteins: chemistry |2 MeSH |
| 650 | _ | 2 | |a tau Proteins: genetics |2 MeSH |
| 650 | _ | 2 | |a tau Proteins: metabolism |2 MeSH |
| 700 | 1 | _ | |a Krüger, Lars |0 P:(DE-2719)2810335 |b 1 |u dzne |
| 700 | 1 | _ | |a Sydow, Astrid |0 P:(DE-2719)2810788 |b 2 |u dzne |
| 700 | 1 | _ | |a Dennissen, Frank Ja |0 P:(DE-2719)2811014 |b 3 |u dzne |
| 700 | 1 | _ | |a Siskova, Zuzana |0 P:(DE-2719)2402361 |b 4 |u dzne |
| 700 | 1 | _ | |a Mandelkow, Eckhard |0 P:(DE-2719)2541671 |b 5 |u dzne |
| 700 | 1 | _ | |a Mandelkow, Eva-Maria |0 P:(DE-2719)2541658 |b 6 |e Last author |u dzne |
| 773 | 1 | 8 | |a 10.15252/embr.201541439 |b : EMBO, 2016-03-01 |n 4 |p 552-569 |3 journal-article |2 Crossref |t EMBO reports |v 17 |y 2016 |x 1469-221X |
| 773 | _ | _ | |a 10.15252/embr.201541439 |g Vol. 17, no. 4, p. 552 - 569 |0 PERI:(DE-600)2025376-X |n 4 |q 17:4<552 - 569 |p 552-569 |t EMBO reports |v 17 |y 2016 |x 1469-221X |
| 856 | 7 | _ | |2 Pubmed Central |u http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4818782 |
| 856 | 4 | _ | |u https://pub.dzne.de/record/138485/files/DZNE-2020-04807_Restricted.pdf |
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| 920 | 1 | _ | |0 I:(DE-2719)1013006 |k AG Remy |l Neuronal Networks |x 1 |
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