Doublecortin expression in CD8+ T-cells and microglia at sites of amyloid-β plaques: A potential role in shaping plaque pathology?
Creators
- 1. Institute of Molecular Regenerative Medicine, Paracelsus Medical University, Salzburg, Austria and Spinal Cord Injury and Tissue Regeneration Center Salzburg (SCI-TReCS), Paracelsus Medical University, Salzburg, Austria
- 2. 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 and Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA
- 3. Institute of Neuroscience, Newcastle University, Newcastle upon Tyne, UK
- 4. Paul Flechsig Institute for Brain Research, University of Leipzig, Leipzig, Germany
- 5. University Hospital Bonn, Clinic and Polyclinic for Neurology, Clinical Neuroscience, Bonn, Germany
- 6. Institute of Molecular Regenerative Medicine, Paracelsus Medical UnivSpinal Cord Injury and Tissue Regeneration Center Salzburg (SCI-TReCS), Paracelsus Medical University, Salzburg, Austria and Institute of Experimental Neuroregeneration, Paracelsus Medical University, Salzburg, Austria
- 7. Department of Neuroscience, School of Medicine, University of California San Diego, San Diego, CA, USA
Description
Abstract
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.
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Unger_AlzDem_2018-P3.pdf
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