000285042 001__ 285042
000285042 005__ 20260209102150.0
000285042 0247_ $$2doi$$a10.1093/brain/awaf462
000285042 0247_ $$2pmid$$apmid:41396874
000285042 0247_ $$2ISSN$$a0006-8950
000285042 0247_ $$2ISSN$$a1460-2156
000285042 037__ $$aDZNE-2026-00166
000285042 041__ $$aEnglish
000285042 082__ $$a610
000285042 1001_ $$0P:(DE-2719)9001924$$aZu, Juan$$b0$$eFirst author$$udzne
000285042 245__ $$aPioglitazone attenuates complement-mediated microglial synaptic engulfment in an Alzheimer's disease model.
000285042 260__ $$aOxford$$bOxford Univ. Press$$c2026
000285042 3367_ $$2DRIVER$$aarticle
000285042 3367_ $$2DataCite$$aOutput Types/Journal article
000285042 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1770628642_24273
000285042 3367_ $$2BibTeX$$aARTICLE
000285042 3367_ $$2ORCID$$aJOURNAL_ARTICLE
000285042 3367_ $$00$$2EndNote$$aJournal Article
000285042 520__ $$aSynaptic loss is an early hallmark of Alzheimer's disease (AD), predominantly driven by aberrant microglial reactivity. Pioglitazone, a peroxisome proliferator-activated receptor gamma (PPAR-γ) agonist with anti-diabetic properties, has been shown to suppress microglial activity and improve cognitive performance in both AD models and clinical studies. However, whether its neuroprotective effects involve direct modulation of synaptic architecture remains unclear. Here, using longitudinal in vivo two-photon imaging, multi-channel immunohistochemistry, super-resolution confocal microscopy and three-dimensional reconstruction techniques in an AD mouse model, we analyse synaptic and microglial interactions. We show that a 4-week pioglitazone treatment preserves dendritic spine density and enhances spine stability over time. Mechanistically, pioglitazone reduces synaptic C1q deposition, thereby limiting complement-mediated microglial synaptic engulfment and attenuating synapse loss. These findings identify pioglitazone as a modulator of complement-dependent microglial synaptic pruning and support its therapeutic potential in preserving synaptic integrity during early AD pathogenesis.
000285042 536__ $$0G:(DE-HGF)POF4-352$$a352 - Disease Mechanisms (POF4-352)$$cPOF4-352$$fPOF IV$$x0
000285042 588__ $$aDataset connected to CrossRef, PubMed, , Journals: pub.dzne.de
000285042 650_7 $$2Other$$aAlzheimer’s disease
000285042 650_7 $$2Other$$amicroglia
000285042 650_7 $$2Other$$aperoxisome proliferator-activated receptor-γ
000285042 650_7 $$2Other$$apioglitazone
000285042 650_7 $$2Other$$asynaptic plasticity
000285042 650_7 $$0X4OV71U42S$$2NLM Chemicals$$aPioglitazone
000285042 650_7 $$080295-33-6$$2NLM Chemicals$$aComplement C1q
000285042 650_7 $$2NLM Chemicals$$aPPAR gamma
000285042 650_2 $$2MeSH$$aPioglitazone: pharmacology
000285042 650_2 $$2MeSH$$aAnimals
000285042 650_2 $$2MeSH$$aAlzheimer Disease: drug therapy
000285042 650_2 $$2MeSH$$aAlzheimer Disease: pathology
000285042 650_2 $$2MeSH$$aAlzheimer Disease: metabolism
000285042 650_2 $$2MeSH$$aMicroglia: drug effects
000285042 650_2 $$2MeSH$$aMicroglia: metabolism
000285042 650_2 $$2MeSH$$aMicroglia: pathology
000285042 650_2 $$2MeSH$$aMice
000285042 650_2 $$2MeSH$$aSynapses: drug effects
000285042 650_2 $$2MeSH$$aSynapses: pathology
000285042 650_2 $$2MeSH$$aDisease Models, Animal
000285042 650_2 $$2MeSH$$aMice, Transgenic
000285042 650_2 $$2MeSH$$aDendritic Spines: drug effects
000285042 650_2 $$2MeSH$$aDendritic Spines: pathology
000285042 650_2 $$2MeSH$$aComplement C1q: metabolism
000285042 650_2 $$2MeSH$$aMice, Inbred C57BL
000285042 650_2 $$2MeSH$$aMale
000285042 650_2 $$2MeSH$$aPPAR gamma: agonists
000285042 650_2 $$2MeSH$$aHumans
000285042 7001_ $$aLi, Cong$$b1
000285042 7001_ $$0P:(DE-2719)9002141$$aCui, Mochen$$b2$$udzne
000285042 7001_ $$0P:(DE-2719)9003588$$aLiu, Xinwu$$b3$$udzne
000285042 7001_ $$0P:(DE-2719)9003796$$aPan, Zhouyang$$b4$$udzne
000285042 7001_ $$0P:(DE-2719)9003834$$aLi, Xiaohe$$b5$$udzne
000285042 7001_ $$0P:(DE-2719)9001979$$aZhang, Fang$$b6$$udzne
000285042 7001_ $$0P:(DE-2719)9002339$$aGentz, Johanna$$b7$$udzne
000285042 7001_ $$aMitteregger-Kretzschmar, Gerda$$b8
000285042 7001_ $$0P:(DE-2719)2810441$$aHerms, Jochen$$b9$$udzne
000285042 7001_ $$0P:(DE-2719)2811433$$aShi, Yuan$$b10$$eLast author
000285042 773__ $$0PERI:(DE-600)1474117-9$$a10.1093/brain/awaf462$$gVol. 149, no. 2, p. 668 - 679$$n2$$p668 - 679$$tBrain$$v149$$x0006-8950$$y2026
000285042 8564_ $$uhttps://pub.dzne.de/record/285042/files/DZNE-2026-00166_Restricted.pdf
000285042 8564_ $$uhttps://pub.dzne.de/record/285042/files/DZNE-2026-00166_Restricted.pdf?subformat=pdfa$$xpdfa
000285042 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)9001924$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b0$$kDZNE
000285042 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)9002141$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b2$$kDZNE
000285042 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)9003588$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b3$$kDZNE
000285042 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)9003796$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b4$$kDZNE
000285042 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)9003834$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b5$$kDZNE
000285042 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)9001979$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b6$$kDZNE
000285042 9101_ $$0I:(DE-HGF)0$$6P:(DE-2719)9002339$$aExternal Institute$$b7$$kExtern
000285042 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2810441$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b9$$kDZNE
000285042 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2811433$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b10$$kDZNE
000285042 9131_ $$0G:(DE-HGF)POF4-352$$1G:(DE-HGF)POF4-350$$2G:(DE-HGF)POF4-300$$3G:(DE-HGF)POF4$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lNeurodegenerative Diseases$$vDisease Mechanisms$$x0
000285042 915__ $$0StatID:(DE-HGF)0420$$2StatID$$aNationallizenz$$d2024-12-12$$wger
000285042 915__ $$0StatID:(DE-HGF)0100$$2StatID$$aJCR$$bBRAIN : 2022$$d2024-12-12
000285042 915__ $$0StatID:(DE-HGF)0200$$2StatID$$aDBCoverage$$bSCOPUS$$d2024-12-12
000285042 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline$$d2024-12-12
000285042 915__ $$0StatID:(DE-HGF)0600$$2StatID$$aDBCoverage$$bEbsco Academic Search$$d2024-12-12
000285042 915__ $$0StatID:(DE-HGF)0030$$2StatID$$aPeer Review$$bASC$$d2024-12-12
000285042 915__ $$0StatID:(DE-HGF)0199$$2StatID$$aDBCoverage$$bClarivate Analytics Master Journal List$$d2024-12-12
000285042 915__ $$0StatID:(DE-HGF)1050$$2StatID$$aDBCoverage$$bBIOSIS Previews$$d2024-12-12
000285042 915__ $$0StatID:(DE-HGF)0160$$2StatID$$aDBCoverage$$bEssential Science Indicators$$d2024-12-12
000285042 915__ $$0StatID:(DE-HGF)1030$$2StatID$$aDBCoverage$$bCurrent Contents - Life Sciences$$d2024-12-12
000285042 915__ $$0StatID:(DE-HGF)1190$$2StatID$$aDBCoverage$$bBiological Abstracts$$d2024-12-12
000285042 915__ $$0StatID:(DE-HGF)1110$$2StatID$$aDBCoverage$$bCurrent Contents - Clinical Medicine$$d2024-12-12
000285042 915__ $$0StatID:(DE-HGF)0113$$2StatID$$aWoS$$bScience Citation Index Expanded$$d2024-12-12
000285042 915__ $$0StatID:(DE-HGF)0150$$2StatID$$aDBCoverage$$bWeb of Science Core Collection$$d2024-12-12
000285042 915__ $$0StatID:(DE-HGF)9910$$2StatID$$aIF >= 10$$bBRAIN : 2022$$d2024-12-12
000285042 9201_ $$0I:(DE-2719)1110001$$kAG Herms$$lTranslational Brain Research$$x0
000285042 980__ $$ajournal
000285042 980__ $$aEDITORS
000285042 980__ $$aVDBINPRINT
000285042 980__ $$aI:(DE-2719)1110001
000285042 980__ $$aUNRESTRICTED