000292292 001__ 292292
000292292 005__ 20240818012520.0
000292292 0247_ $$2doi$$a10.1093/braincomms/fcae256
000292292 0247_ $$2pmid$$apmid:39130515
000292292 0247_ $$2pmc$$apmc:PMC11316205
000292292 0247_ $$2altmetric$$aaltmetric:166252862
000292292 037__ $$aDKFZ-2024-01653
000292292 041__ $$aEnglish
000292292 082__ $$a610
000292292 1001_ $$aCatterson, James H$$b0
000292292 245__ $$aDrosophila appear resistant to trans-synaptic tau propagation.
000292292 260__ $$a[Großbritannien]$$bGuarantors of Brain$$c2024
000292292 3367_ $$2DRIVER$$aarticle
000292292 3367_ $$2DataCite$$aOutput Types/Journal article
000292292 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1723556171_8749
000292292 3367_ $$2BibTeX$$aARTICLE
000292292 3367_ $$2ORCID$$aJOURNAL_ARTICLE
000292292 3367_ $$00$$2EndNote$$aJournal Article
000292292 520__ $$aAlzheimer's disease is the most common cause of dementia in the elderly, prompting extensive efforts to pinpoint novel therapeutic targets for effective intervention. Among the hallmark features of Alzheimer's disease is the development of neurofibrillary tangles comprised of hyperphosphorylated tau protein, whose progressive spread throughout the brain is associated with neuronal death. Trans-synaptic propagation of tau has been observed in mouse models, and indirect evidence for tau spread via synapses has been observed in human Alzheimer's disease. Halting tau propagation is a promising therapeutic target for Alzheimer's disease; thus, a scalable model system to screen for modifiers of tau spread would be very useful for the field. To this end, we sought to emulate the trans-synaptic spread of human tau in Drosophila melanogaster. Employing the trans-Tango circuit mapping technique, we investigated whether tau spreads between synaptically connected neurons. Immunohistochemistry and confocal imaging were used to look for tau propagation. Examination of hundreds of flies expressing four different human tau constructs in two distinct neuronal populations reveals a robust resistance in Drosophila to the trans-synaptic spread of human tau. This resistance persisted in lines with concurrent expression of amyloid-β, in lines with global human tau knock-in to provide a template for human tau in downstream neurons, and with manipulations of temperature. These negative data are important for the field as we establish that Drosophila expressing human tau in subsets of neurons are unlikely to be useful to perform screens to find mechanisms to reduce the trans-synaptic spread of tau. The inherent resistance observed in Drosophila may serve as a valuable clue, offering insights into strategies for impeding tau spread in future studies.
000292292 536__ $$0G:(DE-HGF)POF4-312$$a312 - Funktionelle und strukturelle Genomforschung (POF4-312)$$cPOF4-312$$fPOF IV$$x0
000292292 588__ $$aDataset connected to CrossRef, PubMed, , Journals: inrepo02.dkfz.de
000292292 650_7 $$2Other$$aAlzheimer’s disease
000292292 650_7 $$2Other$$aDrosophila melanogaster
000292292 650_7 $$2Other$$aneurodegeneration
000292292 650_7 $$2Other$$atau
000292292 650_7 $$2Other$$atrans-synaptic
000292292 7001_ $$aMouofo, Edmond N$$b1
000292292 7001_ $$aLópez De Toledo Soler, Inés$$b2
000292292 7001_ $$aLean, Gillian$$b3
000292292 7001_ $$aDlamini, Stella$$b4
000292292 7001_ $$aLiddell, Phoebe$$b5
000292292 7001_ $$aVoong, Graham$$b6
000292292 7001_ $$0P:(DE-He78)f10e8e85107a44f96026964428163c18$$aKatsinelos, Taxiarchis$$b7
000292292 7001_ $$aWang, Yu-Chun$$b8
000292292 7001_ $$aSchoovaerts, Nils$$b9
000292292 7001_ $$00000-0002-5073-5393$$aVerstreken, Patrik$$b10
000292292 7001_ $$00000-0003-2530-0598$$aSpires-Jones, Tara L$$b11
000292292 7001_ $$00000-0001-7552-7358$$aDurrant, Claire S$$b12
000292292 773__ $$0PERI:(DE-600)3020013-1$$a10.1093/braincomms/fcae256$$gVol. 6, no. 4, p. fcae256$$n4$$pfcae256$$tBrain communications$$v6$$x2632-1297$$y2024
000292292 909CO $$ooai:inrepo02.dkfz.de:292292$$pVDB
000292292 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)f10e8e85107a44f96026964428163c18$$aDeutsches Krebsforschungszentrum$$b7$$kDKFZ
000292292 9131_ $$0G:(DE-HGF)POF4-312$$1G:(DE-HGF)POF4-310$$2G:(DE-HGF)POF4-300$$3G:(DE-HGF)POF4$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lKrebsforschung$$vFunktionelle und strukturelle Genomforschung$$x0
000292292 9141_ $$y2024
000292292 915__ $$0StatID:(DE-HGF)0100$$2StatID$$aJCR$$bBRAIN COMMUN : 2022$$d2023-08-24
000292292 915__ $$0StatID:(DE-HGF)0200$$2StatID$$aDBCoverage$$bSCOPUS$$d2023-08-24
000292292 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline$$d2023-08-24
000292292 915__ $$0StatID:(DE-HGF)0320$$2StatID$$aDBCoverage$$bPubMed Central$$d2023-08-24
000292292 915__ $$0StatID:(DE-HGF)0501$$2StatID$$aDBCoverage$$bDOAJ Seal$$d2022-02-21T13:34:18Z
000292292 915__ $$0StatID:(DE-HGF)0500$$2StatID$$aDBCoverage$$bDOAJ$$d2022-02-21T13:34:18Z
000292292 915__ $$0StatID:(DE-HGF)0030$$2StatID$$aPeer Review$$bDOAJ : Anonymous peer review$$d2022-02-21T13:34:18Z
000292292 915__ $$0LIC:(DE-HGF)CCBYNV$$2V:(DE-HGF)$$aCreative Commons Attribution CC BY (No Version)$$bDOAJ$$d2022-02-21T13:34:18Z
000292292 915__ $$0StatID:(DE-HGF)0199$$2StatID$$aDBCoverage$$bClarivate Analytics Master Journal List$$d2023-08-24
000292292 915__ $$0StatID:(DE-HGF)0112$$2StatID$$aWoS$$bEmerging Sources Citation Index$$d2023-08-24
000292292 915__ $$0StatID:(DE-HGF)0150$$2StatID$$aDBCoverage$$bWeb of Science Core Collection$$d2023-08-24
000292292 915__ $$0StatID:(DE-HGF)9900$$2StatID$$aIF < 5$$d2023-08-24
000292292 915__ $$0StatID:(DE-HGF)0561$$2StatID$$aArticle Processing Charges$$d2023-08-24
000292292 915__ $$0StatID:(DE-HGF)0700$$2StatID$$aFees$$d2023-08-24
000292292 9201_ $$0I:(DE-He78)B180-20160331$$kB180$$lProteostase neurodegenerativer Erkrankungen$$x0
000292292 980__ $$ajournal
000292292 980__ $$aVDB
000292292 980__ $$aI:(DE-He78)B180-20160331
000292292 980__ $$aUNRESTRICTED