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@ARTICLE{DelTredici:272672,
      author       = {Del Tredici, Kelly and Schön, Michael and Feldengut,
                      Simone and Ghebremedhin, Estifanos and Kaufman, Sarah K and
                      Wiesner, Diana and Roselli, Francesco and Mayer, Benjamin
                      and Amunts, Katrin and Braak, Heiko},
      title        = {{E}arly {CA}2 {T}au {I}nclusions {D}o {N}ot {D}istinguish
                      an {A}ge-{R}elated {T}auopathy from {E}arly {A}lzheimer's
                      {D}isease.},
      journal      = {Journal of Alzheimer's disease},
      volume       = {101},
      number       = {4},
      issn         = {1387-2877},
      address      = {Amsterdam},
      publisher    = {IOS Press},
      reportid     = {DZNE-2024-01223},
      pages        = {1333 - 1353},
      year         = {2024},
      abstract     = {Neuropathologic 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.},
      keywords     = {Humans / Alzheimer Disease: pathology / Alzheimer Disease:
                      metabolism / Alzheimer Disease: genetics / Female / Aged /
                      Male / Tauopathies: pathology / Tauopathies: metabolism /
                      tau Proteins: metabolism / Aged, 80 and over / Entorhinal
                      Cortex: pathology / Entorhinal Cortex: metabolism / Middle
                      Aged / CA2 Region, Hippocampal: pathology / CA2 Region,
                      Hippocampal: metabolism / Inclusion Bodies: pathology /
                      Inclusion Bodies: metabolism / Neurofibrillary Tangles:
                      pathology / Neurofibrillary Tangles: metabolism / Aging:
                      pathology / Aging: metabolism / APOE (Other) / Alzheimer’s
                      disease (Other) / Ammon’s horn (Other) / CA2 (Other) /
                      PART hypothesis (Other) / entorhinal cortex (Other) /
                      neurofibrillary tangles (Other) / pretangles (Other) / tau
                      seeding (Other) / tractus perforans (Other) / tau Proteins
                      (NLM Chemicals)},
      cin          = {AG Roselli},
      ddc          = {610},
      cid          = {I:(DE-2719)1910001},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39302368},
      doi          = {10.3233/JAD-240483},
      url          = {https://pub.dzne.de/record/272672},
}