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000155769 037__ $$aDZNE-2021-00937
000155769 041__ $$aEnglish
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000155769 1001_ $$0P:(DE-2719)9001545$$aBriel, Nils$$b0$$eFirst author$$udzne
000155769 245__ $$aContribution of the astrocytic tau pathology to synapse loss in progressive supranuclear palsy and corticobasal degeneration.
000155769 260__ $$aOxford$$bWiley-Blackwell$$c2021
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000155769 520__ $$aPrimary 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.
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000155769 650_7 $$2Other$$aastrocytic plaques
000155769 650_7 $$2Other$$acorticobasal degeneration
000155769 650_7 $$2Other$$aprogressive supranuclear palsy
000155769 650_7 $$2Other$$asynapse loss
000155769 650_7 $$2Other$$atauopathy
000155769 650_7 $$2Other$$atufted astrocytes
000155769 650_2 $$2MeSH$$aAged
000155769 650_2 $$2MeSH$$aAged, 80 and over
000155769 650_2 $$2MeSH$$aAstrocytes: pathology
000155769 650_2 $$2MeSH$$aBrain: pathology
000155769 650_2 $$2MeSH$$aCorticobasal Degeneration: pathology
000155769 650_2 $$2MeSH$$aFemale
000155769 650_2 $$2MeSH$$aFrontotemporal Lobar Degeneration: pathology
000155769 650_2 $$2MeSH$$aHumans
000155769 650_2 $$2MeSH$$aInclusion Bodies: pathology
000155769 650_2 $$2MeSH$$aMale
000155769 650_2 $$2MeSH$$aMiddle Aged
000155769 650_2 $$2MeSH$$aNeurons: pathology
000155769 650_2 $$2MeSH$$aSupranuclear Palsy, Progressive: metabolism
000155769 650_2 $$2MeSH$$aSupranuclear Palsy, Progressive: pathology
000155769 650_2 $$2MeSH$$aTauopathies: pathology
000155769 650_2 $$2MeSH$$atau Proteins: metabolism
000155769 7001_ $$0P:(DE-2719)2812307$$aPratsch, Katrin$$b1
000155769 7001_ $$0P:(DE-HGF)0$$aRoeber, Sigrun$$b2
000155769 7001_ $$0P:(DE-2719)2811333$$aArzberger, Thomas$$b3
000155769 7001_ $$0P:(DE-2719)2810441$$aHerms, Jochen$$b4$$eLast author
000155769 773__ $$0PERI:(DE-600)2029927-8$$a10.1111/bpa.12914$$gVol. 31, no. 4$$n4$$pe12914$$tBrain pathology$$v31$$x1750-3639$$y2021
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