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Neural Plasticity
Volume 2017, Article ID 3851262, 15 pages
Research Article

Distinct Pattern of Microgliosis in the Olfactory Bulb of Neurodegenerative Proteinopathies

1Department of Molecular Neurology, Friedrich-Alexander-University Erlangen-Nürnberg, Schwabachanlage 6, 91054 Erlangen, Germany
2Department of Cellular and Molecular Medicine, University of California, La Jolla, San Diego, CA, USA
3Departments of Neurosciences and Pathology, University of California, La Jolla, San Diego, CA, USA
4Department of Neuropathology, Regensburg University Hospital, 93053 Regensburg, Germany

Correspondence should be addressed to Jürgen Winkler; ed.negnalre-ku@relkniw.negreuj and Eliezer Masliah; ude.dscu@hailsame

Received 3 August 2016; Revised 24 November 2016; Accepted 28 December 2016; Published 19 March 2017

Academic Editor: Long-Jun Wu

Copyright © 2017 Zacharias Kohl et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The olfactory bulb (OB) shows early neuropathological hallmarks in numerous neurodegenerative diseases, for example, in Alzheimer’s disease (AD) and Parkinson’s disease (PD). The glomerular and granular cell layer of the OB is characterized by preserved cellular plasticity in the adult brain. In turn, alterations of this cellular plasticity are related to neuroinflammation such as microglia activation, implicated in the pathogenesis of AD and PD, as well as frontotemporal lobe degeneration (FTLD). To determine microglia proliferation and activation we analyzed ionized calcium binding adaptor molecule 1 (Iba1) expressing microglia in the glomerular and granular cell layer, and the olfactory tract of the OB from patients with AD, PD dementia/dementia with Lewy bodies (PDD/DLB), and FTLD compared to age-matched controls. The number of Iba1 and CD68 positive microglia associated with enlarged amoeboid microglia was increased particularly in AD, to a lesser extent in FTLD and PDD/DLB as well, while the proportion of proliferating microglia was not altered. In addition, cells expressing the immature neuronal marker polysialylated neural cell adhesion molecule (PSA-NCAM) were increased in the glomerular layer of PDD/DLB and FTLD cases only. These findings provide novel and detailed insights into differential levels of microglia activation in the OB of neurodegenerative diseases.