000277324 001__ 277324
000277324 005__ 20250323000922.0
000277324 0247_ $$2doi$$a10.3389/fnana.2025.1526962
000277324 0247_ $$2pmid$$apmid:40012738
000277324 0247_ $$2pmc$$apmc:PMC11863279
000277324 0247_ $$2altmetric$$aaltmetric:174928285
000277324 037__ $$aDZNE-2025-00386
000277324 041__ $$aEnglish
000277324 082__ $$a610
000277324 1001_ $$0P:(DE-2719)9001324$$aQu, Tao$$b0$$eFirst author$$udzne
000277324 245__ $$aThe effects of amyloidosis and aging on glutamatergic and GABAergic synapses, and interneurons in the barrel cortex and non-neocortical brain regions.
000277324 260__ $$aLausanne$$bFrontiers Research Foundation$$c2025
000277324 3367_ $$2DRIVER$$aarticle
000277324 3367_ $$2DataCite$$aOutput Types/Journal article
000277324 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1740669970_12645
000277324 3367_ $$2BibTeX$$aARTICLE
000277324 3367_ $$2ORCID$$aJOURNAL_ARTICLE
000277324 3367_ $$00$$2EndNote$$aJournal Article
000277324 520__ $$aPrevious studies on changes in the distribution of GABAergic interneurons and excitation/inhibition (E/I) balance in Alzheimer's disease (AD) and aging were mainly conducted in the neocortex and hippocampus. However, the limbic system is the primary and crucial location for AD progression. Therefore, in this study, we utilized AD and aging mouse models to investigate the E/I balance and the distribution of parvalbumin (PV)- and somatostatin (SST)-expressing cells in S1BF (barrel field of primary somatosensory cortex, barrel cortex), CA1 hippocampal area and brain regions beyond the neocortex and hippocampus, including retrosplenial cortex (RSC, which is composed of RSG and RSA), piriform cortex (Pir), amygdala (BMA), and hypothalamus (DM). We discovered that amyloidosis may disrupt the alignment of excitatory pre- and postsynaptic quantities. Amyloidosis reduces the quantity of synapses and SST cells, but does not impact the counts of PV cells. By contrast, aging is linked to a decline in synapses, I/E ratios, SST and PV cells. Amyloidosis affects the S1BF and BMA, while aging may harm all studied regions, including the S1BF, RSC, hippocampus, Pir, BMA, and DM. Aging mostly affects synapses and I/E ratios in Pir, BMA, and DM, and PV and SST interneurons in the hippocampus.
000277324 536__ $$0G:(DE-HGF)POF4-351$$a351 - Brain Function (POF4-351)$$cPOF4-351$$fPOF IV$$x0
000277324 588__ $$aDataset connected to CrossRef, PubMed, , Journals: pub.dzne.de
000277324 650_7 $$2Other$$aAD
000277324 650_7 $$2Other$$aPV
000277324 650_7 $$2Other$$aSST
000277324 650_7 $$2Other$$aaging
000277324 650_7 $$2Other$$abarrel cortex
000277324 650_7 $$2Other$$anon-neocortical brain regions
000277324 773__ $$0PERI:(DE-600)2452969-2$$a10.3389/fnana.2025.1526962$$gVol. 19, p. 1526962$$p1526962$$tFrontiers in neuroanatomy$$v19$$x1662-5129$$y2025
000277324 8564_ $$uhttps://pub.dzne.de/record/277324/files/DZNE-2025-00386.pdf$$yOpenAccess
000277324 8564_ $$uhttps://pub.dzne.de/record/277324/files/DZNE-2025-00386.pdf?subformat=pdfa$$xpdfa$$yOpenAccess
000277324 909CO $$ooai:pub.dzne.de:277324$$pdnbdelivery$$pdriver$$pVDB$$popen_access$$popenaire
000277324 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)9001324$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b0$$kDZNE
000277324 9131_ $$0G:(DE-HGF)POF4-351$$1G:(DE-HGF)POF4-350$$2G:(DE-HGF)POF4-300$$3G:(DE-HGF)POF4$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lNeurodegenerative Diseases$$vBrain Function$$x0
000277324 9141_ $$y2025
000277324 915__ $$0StatID:(DE-HGF)0200$$2StatID$$aDBCoverage$$bSCOPUS$$d2025-01-06
000277324 915__ $$0StatID:(DE-HGF)0160$$2StatID$$aDBCoverage$$bEssential Science Indicators$$d2025-01-06
000277324 915__ $$0StatID:(DE-HGF)1050$$2StatID$$aDBCoverage$$bBIOSIS Previews$$d2025-01-06
000277324 915__ $$0StatID:(DE-HGF)1190$$2StatID$$aDBCoverage$$bBiological Abstracts$$d2025-01-06
000277324 915__ $$0LIC:(DE-HGF)CCBY4$$2HGFVOC$$aCreative Commons Attribution CC BY 4.0
000277324 915__ $$0StatID:(DE-HGF)0100$$2StatID$$aJCR$$bFRONT NEUROANAT : 2022$$d2025-01-06
000277324 915__ $$0StatID:(DE-HGF)0501$$2StatID$$aDBCoverage$$bDOAJ Seal$$d2024-11-09T09:06:20Z
000277324 915__ $$0StatID:(DE-HGF)0500$$2StatID$$aDBCoverage$$bDOAJ$$d2024-11-09T09:06:20Z
000277324 915__ $$0StatID:(DE-HGF)0113$$2StatID$$aWoS$$bScience Citation Index Expanded$$d2025-01-06
000277324 915__ $$0StatID:(DE-HGF)0700$$2StatID$$aFees$$d2025-01-06
000277324 915__ $$0StatID:(DE-HGF)0150$$2StatID$$aDBCoverage$$bWeb of Science Core Collection$$d2025-01-06
000277324 915__ $$0StatID:(DE-HGF)9900$$2StatID$$aIF < 5$$d2025-01-06
000277324 915__ $$0StatID:(DE-HGF)0510$$2StatID$$aOpenAccess
000277324 915__ $$0StatID:(DE-HGF)0030$$2StatID$$aPeer Review$$bDOAJ : Anonymous peer review$$d2024-11-09T09:06:20Z
000277324 915__ $$0StatID:(DE-HGF)0561$$2StatID$$aArticle Processing Charges$$d2025-01-06
000277324 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline$$d2025-01-06
000277324 915__ $$0StatID:(DE-HGF)0199$$2StatID$$aDBCoverage$$bClarivate Analytics Master Journal List$$d2025-01-06
000277324 9201_ $$0I:(DE-2719)1310007$$kAG Dityatev$$lMolecular Neuroplasticity$$x0
000277324 980__ $$ajournal
000277324 980__ $$aVDB
000277324 980__ $$aUNRESTRICTED
000277324 980__ $$aI:(DE-2719)1310007
000277324 9801_ $$aFullTexts