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Neurosci Res. 2016 May;106:55-61. doi: 10.1016/j.neures.2015.11.006. Epub 2015 Nov 28.

α-Synuclein aggregation in the olfactory bulb of middle-aged common marmoset.

Author information

1
Department of Physiology, Keio University School of Medicine, Shinjuku, Tokyo, Japan.
2
Department of Neuropathology, Brain Bank for Aging Research, Tokyo Metropolitan Institute of Gerontology, Itabashi-ku, Tokyo, Japan.
3
Department of Physiology, Keio University School of Medicine, Shinjuku, Tokyo, Japan; RIKEN Brain Science Institute Laboratory for Marmoset Neural Architecture, Wako-shi, Saitama, Japan.
4
Department of Physiology, Keio University School of Medicine, Shinjuku, Tokyo, Japan; Division of Regenerative Medicine, Jikei University School of Medicine, Minato-ku, Tokyo, Japan.
5
Central Institute for Experimental Animals, Kawasaki, Kanagawa, Japan.
6
Department of Physiology, Keio University School of Medicine, Shinjuku, Tokyo, Japan; RIKEN Brain Science Institute Laboratory for Marmoset Neural Architecture, Wako-shi, Saitama, Japan; Central Institute for Experimental Animals, Kawasaki, Kanagawa, Japan.
7
Department of Physiology, Keio University School of Medicine, Shinjuku, Tokyo, Japan. Electronic address: hidokano@a2.keio.jp.

Abstract

The synaptic protein α-synuclein has been identified as a major component of Lewy bodies, a pathological hallmark of Parkinson's disease (PD). Prior to the formation of Lewy bodies, mislocalization and aggregation of the α-synuclein in brain tissue is frequently observed in various neurodegenerative diseases. Aberrant accumulation and localization of α-synuclein are also observed in the aging human brain, for which reason aging is regarded as a risk factor for neurodegenerative disease. To investigate changes in α-synuclein properties in the aging brain, we compared α-synuclein immunoreactivity in brain tissue of young (2-years-old) and middle-aged (6-years-old) common marmoset (Callithrix jacchus). Our analyses revealed marked changes in α-synuclein immunoreactivity in the olfactory bulb of common marmosets of these age cohorts. Perikaryal α-synuclein aggregations were formed in the olfactory bulb in middle-aged animals. We also observed signals of α-synuclein accumulation in hippocampus in this cohort; however, unlike in the olfactory bulb, hippocampal α-synuclein signals were localized in the synaptic terminals. We did not observe either of these features in younger marmosets, which suggest that aging may play a role in these phenomena. Our results using common marmoset brain corresponded with the observation that the α-synuclein aggregations were first occurred from olfactory bulb in human normal aged and PD brain. Therefore, common marmoset is expected as useful model for α-synuclein pathology.

KEYWORDS:

Common marmoset; Olfactory bulb; Parkinson's disease; α-Synuclein

PMID:
26643383
DOI:
10.1016/j.neures.2015.11.006
[Indexed for MEDLINE]

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