000272672 001__ 272672
000272672 005__ 20241020000055.0
000272672 0247_ $$2doi$$a10.3233/JAD-240483
000272672 0247_ $$2pmid$$apmid:39302368
000272672 0247_ $$2ISSN$$a1387-2877
000272672 0247_ $$2ISSN$$a1875-8908
000272672 0247_ $$2altmetric$$aaltmetric:168095620
000272672 037__ $$aDZNE-2024-01223
000272672 041__ $$aEnglish
000272672 082__ $$a610
000272672 1001_ $$aDel Tredici, Kelly$$b0
000272672 245__ $$aEarly CA2 Tau Inclusions Do Not Distinguish an Age-Related Tauopathy from Early Alzheimer's Disease.
000272672 260__ $$aAmsterdam$$bIOS Press$$c2024
000272672 3367_ $$2DRIVER$$aarticle
000272672 3367_ $$2DataCite$$aOutput Types/Journal article
000272672 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1728913409_2693
000272672 3367_ $$2BibTeX$$aARTICLE
000272672 3367_ $$2ORCID$$aJOURNAL_ARTICLE
000272672 3367_ $$00$$2EndNote$$aJournal Article
000272672 520__ $$aNeuropathologic studies of brains from autopsy series show tau inclusions (pretangles, neuropils threads, neurofibrillary tangles) are detectable more than a decade before amyloid-β (Aβ) deposition in Alzheimer's disease (AD) and develop in a characteristic manner that forms the basis for AD staging. An alternative position views pathological tau without Aβ deposition as a 'primary age-related tauopathy' (PART) rather than prodromal AD. Recently, an early focus of tau inclusions in the Ammon's horn second sector (CA2) with relative sparing of CA1 that occurs before tau inclusions develop in the entorhinal cortex (EC) was proposed as an additional feature of PART.To test the 'definite PART' hypothesis.We used AT8-immunohistochemistry in 100μm sections to examine the EC, transentorhinal cortex (TRE), and Ammon's horn in 325 brains with tau inclusions lacking Aβ deposits (average age at death 66.7 years for females, 66.4 years for males).100% of cases displayed tau inclusions in the TRE. In 89% of cases, the CA1 tau rating was greater than or equal to that in CA2. In 25%, CA2 was devoid of tau inclusions. Only 4% displayed a higher tau score in CA2 than in the TRE, EC, and CA1. The perforant path also displayed early tau changes. APOE genotyping was available for 199/325 individuals. Of these, 44% had an ɛ4 allele that placed them at greater risk for developing later NFT stages and, therefore, clinical AD.Our new findings call into question the PART hypothesis and are consistent with the idea that our cases represent prodromal AD.
000272672 536__ $$0G:(DE-HGF)POF4-352$$a352 - Disease Mechanisms (POF4-352)$$cPOF4-352$$fPOF IV$$x0
000272672 588__ $$aDataset connected to CrossRef, PubMed, , Journals: pub.dzne.de
000272672 650_7 $$2Other$$aAPOE
000272672 650_7 $$2Other$$aAlzheimer’s disease
000272672 650_7 $$2Other$$aAmmon’s horn
000272672 650_7 $$2Other$$aCA2
000272672 650_7 $$2Other$$aPART hypothesis
000272672 650_7 $$2Other$$aentorhinal cortex
000272672 650_7 $$2Other$$aneurofibrillary tangles
000272672 650_7 $$2Other$$apretangles
000272672 650_7 $$2Other$$atau seeding
000272672 650_7 $$2Other$$atractus perforans
000272672 650_7 $$2NLM Chemicals$$atau Proteins
000272672 650_2 $$2MeSH$$aHumans
000272672 650_2 $$2MeSH$$aAlzheimer Disease: pathology
000272672 650_2 $$2MeSH$$aAlzheimer Disease: metabolism
000272672 650_2 $$2MeSH$$aAlzheimer Disease: genetics
000272672 650_2 $$2MeSH$$aFemale
000272672 650_2 $$2MeSH$$aAged
000272672 650_2 $$2MeSH$$aMale
000272672 650_2 $$2MeSH$$aTauopathies: pathology
000272672 650_2 $$2MeSH$$aTauopathies: metabolism
000272672 650_2 $$2MeSH$$atau Proteins: metabolism
000272672 650_2 $$2MeSH$$aAged, 80 and over
000272672 650_2 $$2MeSH$$aEntorhinal Cortex: pathology
000272672 650_2 $$2MeSH$$aEntorhinal Cortex: metabolism
000272672 650_2 $$2MeSH$$aMiddle Aged
000272672 650_2 $$2MeSH$$aCA2 Region, Hippocampal: pathology
000272672 650_2 $$2MeSH$$aCA2 Region, Hippocampal: metabolism
000272672 650_2 $$2MeSH$$aInclusion Bodies: pathology
000272672 650_2 $$2MeSH$$aInclusion Bodies: metabolism
000272672 650_2 $$2MeSH$$aNeurofibrillary Tangles: pathology
000272672 650_2 $$2MeSH$$aNeurofibrillary Tangles: metabolism
000272672 650_2 $$2MeSH$$aAging: pathology
000272672 650_2 $$2MeSH$$aAging: metabolism
000272672 7001_ $$aSchön, Michael$$b1
000272672 7001_ $$aFeldengut, Simone$$b2
000272672 7001_ $$aGhebremedhin, Estifanos$$b3
000272672 7001_ $$aKaufman, Sarah K$$b4
000272672 7001_ $$0P:(DE-2719)2812844$$aWiesner, Diana$$b5$$udzne
000272672 7001_ $$0P:(DE-2719)2812851$$aRoselli, Francesco$$b6$$udzne
000272672 7001_ $$aMayer, Benjamin$$b7
000272672 7001_ $$aAmunts, Katrin$$b8
000272672 7001_ $$aBraak, Heiko$$b9
000272672 773__ $$0PERI:(DE-600)2070772-1$$a10.3233/JAD-240483$$gVol. 101, no. 4, p. 1333 - 1353$$n4$$p1333 - 1353$$tJournal of Alzheimer's disease$$v101$$x1387-2877$$y2024
000272672 8564_ $$uhttps://pub.dzne.de/record/272672/files/DZNE-2024-01223_Restricted.pdf
000272672 8564_ $$uhttps://pub.dzne.de/record/272672/files/DZNE-2024-01223_Supp.pdf
000272672 8564_ $$uhttps://pub.dzne.de/record/272672/files/DZNE-2024-01223_Restricted.pdf?subformat=pdfa$$xpdfa
000272672 8564_ $$uhttps://pub.dzne.de/record/272672/files/DZNE-2024-01223_Supp.pdf?subformat=pdfa$$xpdfa
000272672 909CO $$ooai:pub.dzne.de:272672$$pVDB
000272672 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2812844$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b5$$kDZNE
000272672 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2812851$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b6$$kDZNE
000272672 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
000272672 9141_ $$y2024
000272672 915__ $$0StatID:(DE-HGF)0100$$2StatID$$aJCR$$bJ ALZHEIMERS DIS : 2022$$d2023-08-25
000272672 915__ $$0StatID:(DE-HGF)0200$$2StatID$$aDBCoverage$$bSCOPUS$$d2023-08-25
000272672 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline$$d2023-08-25
000272672 915__ $$0StatID:(DE-HGF)0600$$2StatID$$aDBCoverage$$bEbsco Academic Search$$d2023-08-25
000272672 915__ $$0StatID:(DE-HGF)0030$$2StatID$$aPeer Review$$bASC$$d2023-08-25
000272672 915__ $$0StatID:(DE-HGF)0199$$2StatID$$aDBCoverage$$bClarivate Analytics Master Journal List$$d2023-08-25
000272672 915__ $$0StatID:(DE-HGF)1050$$2StatID$$aDBCoverage$$bBIOSIS Previews$$d2023-08-25
000272672 915__ $$0StatID:(DE-HGF)0113$$2StatID$$aWoS$$bScience Citation Index Expanded$$d2023-08-25
000272672 915__ $$0StatID:(DE-HGF)0150$$2StatID$$aDBCoverage$$bWeb of Science Core Collection$$d2023-08-25
000272672 915__ $$0StatID:(DE-HGF)1030$$2StatID$$aDBCoverage$$bCurrent Contents - Life Sciences$$d2023-08-25
000272672 915__ $$0StatID:(DE-HGF)1190$$2StatID$$aDBCoverage$$bBiological Abstracts$$d2023-08-25
000272672 915__ $$0StatID:(DE-HGF)0160$$2StatID$$aDBCoverage$$bEssential Science Indicators$$d2023-08-25
000272672 915__ $$0StatID:(DE-HGF)9900$$2StatID$$aIF < 5$$d2023-08-25
000272672 9201_ $$0I:(DE-2719)1910001$$kAG Roselli$$lMetabolic Changes in Neurodegeneration$$x0
000272672 980__ $$ajournal
000272672 980__ $$aVDB
000272672 980__ $$aI:(DE-2719)1910001
000272672 980__ $$aUNRESTRICTED