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Decreased hippocampal cell proliferation in mice with experimental antiphospholipid syndrome


Frauenknecht, Katrin; Leukel, Petra; Weiss, Ronen; von Pein, Harald D; Katzav, Aviva; Chapman, Joab; Sommer, Clemens J (2018). Decreased hippocampal cell proliferation in mice with experimental antiphospholipid syndrome. Brain Structure & Function, 223(7):3463-3471.

Abstract

The antiphospholipid syndrome (APS) is an autoimmune disease characterized by the presence of antiphospholipid antibodies, which may trigger vascular thrombosis with consecutive infarcts. However, cognitive dysfunctions representing one of the most commonest neuropsychiatric symptoms are frequently present despite the absence of any ischemic brain lesions. Data on the structural and functional basis of the neuropsychiatric symptoms are sparse. To examine the effect of APS on hippocampal neurogenesis and on white matter, we induced experimental APS (eAPS) in adult female Balb/C mice by immunization with β2-glycoprotein 1. To investigate cell proliferation in the dentate gyrus granular cell layer (DG GCL), eAPS and control mice (n = 5, each) were injected with 5-bromo-2′-deoxyuridine (BrdU) once a day for 10 subsequent days. Sixteen weeks after immunization, eAPS resulted in a significant reduction of BrdU-positive cells in the DG GCL compared to control animals. However, double staining with doublecortin and NeuN revealed a largely preserved neurogenesis. Ultrastructural analysis of corpus callosum (CC) axons in eAPS (n = 6) and control mice (n = 7) revealed no significant changes in CC axon diameter or g-ratio. In conclusion, decreased cellular proliferation in the hippocampus of eAPS mice indicates a limited regenerative potential and may represent one neuropathological substrate of cognitive changes in APS while evidence for alterations of white matter integrity is lacking.
Keywords Antiphospholipid syndrome Corpus callosum g-ratio BrdU Neurogenesis

Abstract

The antiphospholipid syndrome (APS) is an autoimmune disease characterized by the presence of antiphospholipid antibodies, which may trigger vascular thrombosis with consecutive infarcts. However, cognitive dysfunctions representing one of the most commonest neuropsychiatric symptoms are frequently present despite the absence of any ischemic brain lesions. Data on the structural and functional basis of the neuropsychiatric symptoms are sparse. To examine the effect of APS on hippocampal neurogenesis and on white matter, we induced experimental APS (eAPS) in adult female Balb/C mice by immunization with β2-glycoprotein 1. To investigate cell proliferation in the dentate gyrus granular cell layer (DG GCL), eAPS and control mice (n = 5, each) were injected with 5-bromo-2′-deoxyuridine (BrdU) once a day for 10 subsequent days. Sixteen weeks after immunization, eAPS resulted in a significant reduction of BrdU-positive cells in the DG GCL compared to control animals. However, double staining with doublecortin and NeuN revealed a largely preserved neurogenesis. Ultrastructural analysis of corpus callosum (CC) axons in eAPS (n = 6) and control mice (n = 7) revealed no significant changes in CC axon diameter or g-ratio. In conclusion, decreased cellular proliferation in the hippocampus of eAPS mice indicates a limited regenerative potential and may represent one neuropathological substrate of cognitive changes in APS while evidence for alterations of white matter integrity is lacking.
Keywords Antiphospholipid syndrome Corpus callosum g-ratio BrdU Neurogenesis

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Institute of Neuropathology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Scopus Subject Areas:Health Sciences > Anatomy
Life Sciences > General Neuroscience
Health Sciences > Histology
Uncontrolled Keywords:Anatomy, General Neuroscience, Histology
Language:English
Date:1 September 2018
Deposited On:11 Jan 2019 08:06
Last Modified:29 Jul 2020 08:53
Publisher:Springer
ISSN:1863-2653
Additional Information:This is a post-peer-review, pre-copyedit version of an article published in Brain Struct Funct. The final authenticated version is available online at: https://doi.org/10.1007/s00429-018-1699-9
OA Status:Green
Publisher DOI:https://doi.org/10.1007/s00429-018-1699-9
PubMed ID:29936552
Project Information:
  • : FunderStavros Niarchos Foundation
  • : Grant ID
  • : Project Title

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