Doublecortin expression in CD8+ T-cells and microglia at sites of amyloid-β plaques: A potential role in shaping plaque pathology?
Autor: | Unger MS; Institute of Molecular Regenerative Medicine, Paracelsus Medical University, Salzburg, Austria; Spinal Cord Injury and Tissue Regeneration Center Salzburg (SCI-TReCS), Paracelsus Medical University, Salzburg, Austria., Marschallinger J; Institute of Molecular Regenerative Medicine, Paracelsus Medical University, Salzburg, Austria; Spinal Cord Injury and Tissue Regeneration Center Salzburg (SCI-TReCS), Paracelsus Medical University, Salzburg, Austria; Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA., Kaindl J; Institute of Molecular Regenerative Medicine, Paracelsus Medical University, Salzburg, Austria; Spinal Cord Injury and Tissue Regeneration Center Salzburg (SCI-TReCS), Paracelsus Medical University, Salzburg, Austria., Klein B; Institute of Molecular Regenerative Medicine, Paracelsus Medical University, Salzburg, Austria; Spinal Cord Injury and Tissue Regeneration Center Salzburg (SCI-TReCS), Paracelsus Medical University, Salzburg, Austria., Johnson M; Institute of Neuroscience, Newcastle University, Newcastle upon Tyne, UK., Khundakar AA; Institute of Neuroscience, Newcastle University, Newcastle upon Tyne, UK., Roßner S; Paul Flechsig Institute for Brain Research, University of Leipzig, Leipzig, Germany., Heneka MT; University Hospital Bonn, Clinic and Polyclinic for Neurology, Clinical Neuroscience, Bonn, Germany., Couillard-Despres S; Spinal Cord Injury and Tissue Regeneration Center Salzburg (SCI-TReCS), Paracelsus Medical University, Salzburg, Austria; Institute of Experimental Neuroregeneration, Paracelsus Medical University, Salzburg, Austria., Rockenstein E; Department of Neuroscience, School of Medicine, University of California San Diego, San Diego, CA, USA., Masliah E; Department of Neuroscience, School of Medicine, University of California San Diego, San Diego, CA, USA., Attems J; Institute of Neuroscience, Newcastle University, Newcastle upon Tyne, UK., Aigner L; Institute of Molecular Regenerative Medicine, Paracelsus Medical University, Salzburg, Austria; Spinal Cord Injury and Tissue Regeneration Center Salzburg (SCI-TReCS), Paracelsus Medical University, Salzburg, Austria. Electronic address: ludwig.aigner@pmu.ac.at. |
---|---|
Jazyk: | angličtina |
Zdroj: | Alzheimer's & dementia : the journal of the Alzheimer's Association [Alzheimers Dement] 2018 Aug; Vol. 14 (8), pp. 1022-1037. Date of Electronic Publication: 2018 Apr 07. |
DOI: | 10.1016/j.jalz.2018.02.017 |
Abstrakt: | Introduction: One characteristic of Alzheimer's disease is the formation of amyloid-β plaques, which are typically linked to neuroinflammation and surrounded by inflammatory cells such as microglia and infiltrating immune cells. Methods: Here, we describe nonneurogenic doublecortin (DCX) positive cells, DCX being generally used as a marker for young immature neurons, at sites of amyloid-β plaques in various transgenic amyloid mouse models and in human brains with plaque pathology. Results: The plaque-associated DCX+ cells were not of neurogenic identity, instead most of them showed coexpression with markers for microglia (ionized calcium-binding adapter molecule 1) and for phagocytosis (CD68 and TREM2). Another subpopulation of plaque-associated DCX+ cells was negative for ionized calcium-binding adapter molecule 1 but was highly positive for the pan-leukocyte marker CD45. These hematopoietic cells were identified as CD3-and CD8-positive and CD4-negative T-cells. Discussion: Peculiarly, the DCX+/ionized calcium-binding adapter molecule 1+ microglia and DCX+/CD8+ T-cells were closely attached, suggesting that these two cell types are tightly interacting and that this interaction might shape plaque pathology. (Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.) |
Databáze: | MEDLINE |
Externí odkaz: |