Tags

Type your tag names separated by a space and hit enter

Expression of α-synuclein is regulated in a neuronal cell type-dependent manner.
Anat Sci Int. 2019 Jan; 94(1):11-22.AS

Abstract

α-Synuclein, the major component of Lewy bodies (LBs) and Lewy neurites (LNs), is expressed in presynapses under physiologically normal conditions and is involved in synaptic function. Abnormal intracellular aggregates of misfolded α-synuclein such as LBs and LNs are pathological hallmarks of synucleinopathies, including Parkinson's disease (PD) and dementia with Lewy bodies (DLB). According to previous studies using pathological models overexpressing α-synuclein, high expression of this protein in neurons is a critical risk factor for neurodegeneration. Therefore, it is important to know the endogenous expression levels of α-synuclein in each neuronal cell type. We previously reported differential expression profiles of α-synuclein in vitro and in vivo. In the wild-type mouse brain, particularly in vulnerable regions affected during the progression of idiopathic PD, α-synuclein is highly expressed in neuronal cell bodies of some early PD-affected regions, such as the olfactory bulb, the dorsal motor nucleus of the vagus, and the substantia nigra pars compacta. Synaptic expression of α-synuclein is mostly accompanied by expression of vesicular glutamate transporter-1, an excitatory synapse marker protein. In contrast, α-synuclein expression in inhibitory synapses differs among brain regions. Recently accumulated evidence indicates the close relationship between differential expression profiles of α-synuclein and selective vulnerability of certain neuronal populations. Further studies on the regulation of α-synuclein expression will help to understand the mechanism of LB pathology and provide an innovative therapeutic strategy to prevent PD and DLB onset.

Links

PMC Free PDF

Authors+Show Affiliations

Taguchi K
Department of Anatomy and Neurobiology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kawaramachi-Hirokoji, Kamikyo-ku, Kyoto, 602-8566, Japan.
Watanabe Y
Department of Basic Geriatrics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kawaramachi-Hirokoji, Kamikyo-ku, Kyoto, 602-8566, Japan.
Tsujimura A
Department of Basic Geriatrics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kawaramachi-Hirokoji, Kamikyo-ku, Kyoto, 602-8566, Japan.
Tanaka M
Department of Anatomy and Neurobiology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kawaramachi-Hirokoji, Kamikyo-ku, Kyoto, 602-8566, Japan. mtanaka@koto.kpu-m.ac.jp.

MeSH

AnimalsBrainGene Expression RegulationHumansLewy BodiesLewy Body DiseaseMiceNeuronsParkinson DiseaseProtein Foldingalpha-Synuclein

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

30362073

Citation

Taguchi, Katsutoshi, et al. "Expression of Α-synuclein Is Regulated in a Neuronal Cell Type-dependent Manner." Anatomical Science International, vol. 94, no. 1, 2019, pp. 11-22.
Taguchi K, Watanabe Y, Tsujimura A, et al. Expression of α-synuclein is regulated in a neuronal cell type-dependent manner. Anat Sci Int. 2019;94(1):11-22.
Taguchi, K., Watanabe, Y., Tsujimura, A., & Tanaka, M. (2019). Expression of α-synuclein is regulated in a neuronal cell type-dependent manner. Anatomical Science International, 94(1), 11-22. https://doi.org/10.1007/s12565-018-0464-8
Taguchi K, et al. Expression of Α-synuclein Is Regulated in a Neuronal Cell Type-dependent Manner. Anat Sci Int. 2019;94(1):11-22. PubMed PMID: 30362073.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Expression of α-synuclein is regulated in a neuronal cell type-dependent manner. AU - Taguchi,Katsutoshi, AU - Watanabe,Yoshihisa, AU - Tsujimura,Atsushi, AU - Tanaka,Masaki, Y1 - 2018/10/25/ PY - 2018/08/22/received PY - 2018/10/14/accepted PY - 2018/10/27/pubmed PY - 2019/4/17/medline PY - 2018/10/27/entrez KW - Dementia with Lewy bodies KW - Excitatory neuron KW - Inhibitory neuron KW - Parkinson’s disease KW - Synapse SP - 11 EP - 22 JF - Anatomical science international JO - Anat Sci Int VL - 94 IS - 1 N2 - α-Synuclein, the major component of Lewy bodies (LBs) and Lewy neurites (LNs), is expressed in presynapses under physiologically normal conditions and is involved in synaptic function. Abnormal intracellular aggregates of misfolded α-synuclein such as LBs and LNs are pathological hallmarks of synucleinopathies, including Parkinson's disease (PD) and dementia with Lewy bodies (DLB). According to previous studies using pathological models overexpressing α-synuclein, high expression of this protein in neurons is a critical risk factor for neurodegeneration. Therefore, it is important to know the endogenous expression levels of α-synuclein in each neuronal cell type. We previously reported differential expression profiles of α-synuclein in vitro and in vivo. In the wild-type mouse brain, particularly in vulnerable regions affected during the progression of idiopathic PD, α-synuclein is highly expressed in neuronal cell bodies of some early PD-affected regions, such as the olfactory bulb, the dorsal motor nucleus of the vagus, and the substantia nigra pars compacta. Synaptic expression of α-synuclein is mostly accompanied by expression of vesicular glutamate transporter-1, an excitatory synapse marker protein. In contrast, α-synuclein expression in inhibitory synapses differs among brain regions. Recently accumulated evidence indicates the close relationship between differential expression profiles of α-synuclein and selective vulnerability of certain neuronal populations. Further studies on the regulation of α-synuclein expression will help to understand the mechanism of LB pathology and provide an innovative therapeutic strategy to prevent PD and DLB onset. SN - 1447-073X UR - https://www.unboundmedicine.com/medline/citation/30362073/Expression_of_α_synuclein_is_regulated_in_a_neuronal_cell_type_dependent_manner_ DB - PRIME DP - Unbound Medicine ER -