gms | German Medical Science

60. Jahrestagung der Deutschen Gesellschaft für Neuropathologie und Neuroanatomie (DGNN)

Deutsche Gesellschaft für Neuropathologie und Neuroanatomie

26. - 28.08.2015, Berlin

Microglial (dys)function in Alzheimer’s disease-like mice harboring defined Aβ species

Meeting Abstract

Suche in Medline nach

  • corresponding author presenting/speaker Stefanie Seifert - Charité Berlin, Department of Neuropathology, Berlin, Germany
  • Debora Pehl - Charité Berlin, Department of Neuropathology, Berlin, Germany
  • Stefan Prokop - Charité Berlin, Department of Neuropathology, Berlin, Germany
  • Frank L. Heppner - Charité Berlin, Department of Neuropathology, Berlin, Germany

Deutsche Gesellschaft für Neuropathologie und Neuroanatomie. 60th Annual Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN). Berlin, 26.-28.08.2015. Düsseldorf: German Medical Science GMS Publishing House; 2015. Doc15dgnnP5

doi: 10.3205/15dgnn29, urn:nbn:de:0183-15dgnn299

Veröffentlicht: 25. August 2015

© 2015 Seifert et al.
Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung). Lizenz-Angaben siehe http://creativecommons.org/licenses/by/4.0/.


Gliederung

Text

A major pathophysiological hallmark of Alzheimer’s disease (AD) is the generation and deposition of cerebral β amyloid (Aß). Recently, we showed that microglia cells obtain an impaired function in an Aβ-dependent manner, as shown by a decrease in microglial phagocytic activity and directed process motility in Aβ depositing APPPS1 and APP23 mice [1]. Since various species and aggregation states of Aβ co-exist, most likely with varying pathogenic impact, we extended our analyses of microglial (dys)function in AD-like mouse models by investigating “oligomeric” AD-like mice carrying the Dutch mutation in the APP gene [2]. Given that these mice exhibit oligomeric Aß species and show no Aβ plaque deposition while having changes in cognition, our data will provide a better understanding of – potentially pathogenically relevant – microglial actions in AD.


References

1.
Krabbe G, Halle A, Matyash V, Rinnenthal JL, Eom GD, Bernhardt U, Miller KR, Prokop S, Kettenmann H, Heppner FL. Functional impairment of microglia coincides with Beta-amyloid deposition in mice with Alzheimer-like pathology. PLoS One. 2013;8(4):e60921. DOI: 10.1371/journal.pone.0060921 Externer Link
2.
Gandy S, Simon AJ, Steele JW, Lublin AL, Lah JJ, Walker LC, Levey AI, Krafft GA, Levy E, Checler F, Glabe C, Bilker WB, Abel T, Schmeidler J, Ehrlich ME. Days to criterion as an indicator of toxicity associated with human Alzheimer amyloid-beta oligomers. Ann Neurol. 2010 Aug;68(2):220-30. DOI: 10.1002/ana.22052 Externer Link