Home > Publications Database > Contribution of the astrocytic tau pathology to synapse loss in progressive supranuclear palsy and corticobasal degeneration. > print

001     155769
005     20240403115640.0
024 7 _ |a 10.1111/bpa.12914
|2 doi
024 7 _ |a pmid:33089580
|2 pmid
024 7 _ |a pmc:PMC8412068
|2 pmc
024 7 _ |a 1015-6305
|2 ISSN
024 7 _ |a 1750-3639
|2 ISSN
024 7 _ |a altmetric:93083029
|2 altmetric
037 _ _ |a DZNE-2021-00937
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Briel, Nils
|0 P:(DE-2719)9001545
|b 0
|e First author
|u dzne
245 _ _ |a Contribution of the astrocytic tau pathology to synapse loss in progressive supranuclear palsy and corticobasal degeneration.
260 _ _ |a Oxford
|c 2021
|b Wiley-Blackwell
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 1712134327_27007
|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 Primary 4-repeat tauopathies with frontotemporal lobar degeneration (FTLD) like Progressive Supranuclear Palsy (PSP) or Corticobasal Degeneration (CBD) show diverse cellular pathology in various brain regions. Besides shared characteristics of neuronal and oligodendroglial cytoplasmic inclusions of accumulated hyperphosphorylated tau protein (pTau), astrocytes in PSP and CBD contain pathognomonic pTau aggregates - hence, lending the designation tufted astrocytes (TA) or astrocytic plaques (AP), respectively. pTau toxicity is most commonly assigned to neurons, whereas the implications of astrocytic pTau for maintaining neurotransmission within the tripartite synapse of human brains is not well understood. We performed immunofluorescent synapse labeling and automated puncta quantification in the medial frontal gyrus (MFG) and striatal regions from PSP and CBD postmortem samples to capture morphometric synaptic alterations. This approach indicated general synaptic losses of both, excitatory and inhibitory bipartite synapses in the frontal cortex of PSP cases, whereas in CBD lower synapse densities were only related to astrocytic plaques. In contrast to tufted astrocytes in PSP, affected astrocytes in CBD could not preserve synaptic integrity within their spatial domains, when compared to non-affected internal astrocytes or astrocytes in healthy controls. These findings suggest a pTau pathology-associated role of astrocytes in maintaining connections within neuronal circuits, considered as the microscopic substrate of cognitive dysfunction in CBD. By contrasting astrocytic-synaptic associations in both diseases, we hereby highlight astrocytic pTau as an important subject of prospective research and as a potential cellular target for therapeutic approaches in the primary tauopathies PSP and CBD.
536 _ _ |a 352 - Disease Mechanisms (POF4-352)
|0 G:(DE-HGF)POF4-352
|c POF4-352
|f POF IV
|x 0
588 _ _ |a Dataset connected to CrossRef, PubMed, , Journals: pub.dzne.de
650 _ 7 |a astrocytic plaques
|2 Other
650 _ 7 |a corticobasal degeneration
|2 Other
650 _ 7 |a progressive supranuclear palsy
|2 Other
650 _ 7 |a synapse loss
|2 Other
650 _ 7 |a tauopathy
|2 Other
650 _ 7 |a tufted astrocytes
|2 Other
650 _ 2 |a Aged
|2 MeSH
650 _ 2 |a Aged, 80 and over
|2 MeSH
650 _ 2 |a Astrocytes: pathology
|2 MeSH
650 _ 2 |a Brain: pathology
|2 MeSH
650 _ 2 |a Corticobasal Degeneration: pathology
|2 MeSH
650 _ 2 |a Female
|2 MeSH
650 _ 2 |a Frontotemporal Lobar Degeneration: pathology
|2 MeSH
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Inclusion Bodies: pathology
|2 MeSH
650 _ 2 |a Male
|2 MeSH
650 _ 2 |a Middle Aged
|2 MeSH
650 _ 2 |a Neurons: pathology
|2 MeSH
650 _ 2 |a Supranuclear Palsy, Progressive: metabolism
|2 MeSH
650 _ 2 |a Supranuclear Palsy, Progressive: pathology
|2 MeSH
650 _ 2 |a Tauopathies: pathology
|2 MeSH
650 _ 2 |a tau Proteins: metabolism
|2 MeSH
700 1 _ |a Pratsch, Katrin
|0 P:(DE-2719)2812307
|b 1
700 1 _ |a Roeber, Sigrun
|0 P:(DE-HGF)0
|b 2
700 1 _ |a Arzberger, Thomas
|0 P:(DE-2719)2811333
|b 3
700 1 _ |a Herms, Jochen
|0 P:(DE-2719)2810441
|b 4
|e Last author
773 _ _ |a 10.1111/bpa.12914
|g Vol. 31, no. 4
|0 PERI:(DE-600)2029927-8
|n 4
|p e12914
|t Brain pathology
|v 31
|y 2021
|x 1750-3639
856 4 _ |y OpenAccess
|u https://pub.dzne.de/record/155769/files/DZNE-2021-00937.pdf
856 4 _ |y OpenAccess
|x pdfa
|u https://pub.dzne.de/record/155769/files/DZNE-2021-00937.pdf?subformat=pdfa
909 C O |o oai:pub.dzne.de:155769
|p openaire
|p open_access
|p VDB
|p driver
|p dnbdelivery
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 0
|6 P:(DE-2719)9001545
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 1
|6 P:(DE-2719)2812307
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 3
|6 P:(DE-2719)2811333
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 4
|6 P:(DE-2719)2810441
913 1 _ |a DE-HGF
|b Gesundheit
|l Neurodegenerative Diseases
|1 G:(DE-HGF)POF4-350
|0 G:(DE-HGF)POF4-352
|3 G:(DE-HGF)POF4
|2 G:(DE-HGF)POF4-300
|4 G:(DE-HGF)POF
|v Disease Mechanisms
|x 0
914 1 _ |y 2021
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0150
|2 StatID
|b Web of Science Core Collection
|d 2022-11-17
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0160
|2 StatID
|b Essential Science Indicators
|d 2021-02-02
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1050
|2 StatID
|b BIOSIS Previews
|d 2022-11-17
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1190
|2 StatID
|b Biological Abstracts
|d 2021-02-02
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0600
|2 StatID
|b Ebsco Academic Search
|d 2022-11-17
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0501
|2 StatID
|b DOAJ Seal
|d 2022-09-26T13:10:13Z
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1030
|2 StatID
|b Current Contents - Life Sciences
|d 2022-11-17
915 _ _ |a IF >= 5
|0 StatID:(DE-HGF)9905
|2 StatID
|b BRAIN PATHOL : 2021
|d 2022-11-17
915 _ _ |a DEAL Wiley
|0 StatID:(DE-HGF)3001
|2 StatID
|d 2021-02-02
|w ger
915 _ _ |a WoS
|0 StatID:(DE-HGF)0113
|2 StatID
|b Science Citation Index Expanded
|d 2021-02-02
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0500
|2 StatID
|b DOAJ
|d 2022-09-26T13:10:13Z
915 _ _ |a OpenAccess
|0 StatID:(DE-HGF)0510
|2 StatID
915 _ _ |a Peer Review
|0 StatID:(DE-HGF)0030
|2 StatID
|b ASC
|d 2022-11-17
915 _ _ |a JCR
|0 StatID:(DE-HGF)0100
|2 StatID
|b BRAIN PATHOL : 2021
|d 2022-11-17
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0300
|2 StatID
|b Medline
|d 2022-11-17
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0200
|2 StatID
|b SCOPUS
|d 2022-11-17
915 _ _ |a Creative Commons Attribution CC BY 4.0
|0 LIC:(DE-HGF)CCBY4
|2 HGFVOC
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0199
|2 StatID
|b Clarivate Analytics Master Journal List
|d 2022-11-17
920 1 _ |0 I:(DE-2719)1110001
|k AG Herms
|l Translational Brain Research
|x 0
920 1 _ |0 I:(DE-2719)1140013
|k Neuropathology / Brainbank
|l Neuropathology / Brainbank
|x 1
980 _ _ |a journal
980 _ _ |a VDB
980 _ _ |a UNRESTRICTED
980 _ _ |a I:(DE-2719)1110001
980 _ _ |a I:(DE-2719)1140013
980 1 _ |a FullTexts

LibraryCollectionCLSMajorCLSMinorLanguageAuthor
Marc 21