Interaction between Neuromelanin and Alpha-Synuclein in Parkinson’s Disease
Identifieur interne : 000393 ( Ncbi/Merge ); précédent : 000392; suivant : 000394Interaction between Neuromelanin and Alpha-Synuclein in Parkinson’s Disease
Auteurs : Shengli Xu [République populaire de Chine] ; Piu Chan [République populaire de Chine]Source :
- Biomolecules [ 2218-273X ] ; 2015.
Abstract
Parkinson’s disease (PD) is a very common neurodegenerative disorder characterized by the accumulation of α-synuclein (α-syn) into Lewy body (LB) inclusions and the loss of neuronmelanin (NM) containing dopamine (DA) neurons in the substantia nigra (SN). Pathological α-syn and NM are two prominent hallmarks in this selective and progressive neurodegenerative disease. Pathological α-syn can induce dopaminergic neuron death by various mechanisms, such as inducing oxidative stress and inhibiting protein degradation systems. Therefore, to explore the factors that trigger α-syn to convert from a non-toxic protein to toxic one is a pivotal question to clarify the mechanisms of PD pathogenesis. Many triggers for pathological α-syn aggregation have been identified, including missense mutations in the α-syn gene, higher concentration, and posttranslational modifications of α-Syn. Recently, the role of NM in inducing α-syn expression and aggregation has been suggested as a mechanism for this pigment to modulate neuronal vulnerability in PD. NM may be responsible for PD and age-associated increase and aggregation in α-syn. Here, we reviewed our previous study and other recent findings in the area of interaction between NM and α-syn.
Url:
DOI: 10.3390/biom5021122
PubMed: 26057626
PubMed Central: 4496713
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<affiliation><nlm:aff id="af1-biomolecules-05-01122">Beijing Institute of Geriatrics, Xuanwu Hospital of Capital University of Medical Sciences, No.45 changchun St., Xicheng District, Beijing 100053, China; E-Mail:<email>xushngli_xw@163.com</email>
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<front><div type="abstract" xml:lang="en"><p>Parkinson’s disease (PD) is a very common neurodegenerative disorder characterized by the accumulation of α-synuclein (α-syn) into Lewy body (LB) inclusions and the loss of neuronmelanin (NM) containing dopamine (DA) neurons in the substantia nigra (SN). Pathological α-syn and NM are two prominent hallmarks in this selective and progressive neurodegenerative disease. Pathological α-syn can induce dopaminergic neuron death by various mechanisms, such as inducing oxidative stress and inhibiting protein degradation systems. Therefore, to explore the factors that trigger α-syn to convert from a non-toxic protein to toxic one is a pivotal question to clarify the mechanisms of PD pathogenesis. Many triggers for pathological α-syn aggregation have been identified, including missense mutations in the α-syn gene, higher concentration, and posttranslational modifications of α-Syn. Recently, the role of NM in inducing α-syn expression and aggregation has been suggested as a mechanism for this pigment to modulate neuronal vulnerability in PD. NM may be responsible for PD and age-associated increase and aggregation in α-syn. Here, we reviewed our previous study and other recent findings in the area of interaction between NM and α-syn.</p>
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<pmc article-type="review-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Biomolecules</journal-id>
<journal-id journal-id-type="iso-abbrev">Biomolecules</journal-id>
<journal-id journal-id-type="publisher-id">biomolecules</journal-id>
<journal-title-group><journal-title>Biomolecules</journal-title>
</journal-title-group>
<issn pub-type="epub">2218-273X</issn>
<publisher><publisher-name>MDPI</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">26057626</article-id>
<article-id pub-id-type="pmc">4496713</article-id>
<article-id pub-id-type="doi">10.3390/biom5021122</article-id>
<article-id pub-id-type="publisher-id">biomolecules-05-01122</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Review</subject>
</subj-group>
</article-categories>
<title-group><article-title>Interaction between Neuromelanin and Alpha-Synuclein in Parkinson’s Disease</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Xu</surname>
<given-names>Shengli</given-names>
</name>
<xref ref-type="aff" rid="af1-biomolecules-05-01122">1</xref>
<xref ref-type="aff" rid="af2-biomolecules-05-01122">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Chan</surname>
<given-names>Piu</given-names>
</name>
<xref ref-type="aff" rid="af1-biomolecules-05-01122">1</xref>
<xref ref-type="aff" rid="af2-biomolecules-05-01122">2</xref>
<xref rid="c1-biomolecules-05-01122" ref-type="corresp">*</xref>
</contrib>
</contrib-group>
<contrib-group><contrib contrib-type="editor"><name><surname>Witt</surname>
<given-names>Stephan N.</given-names>
</name>
<role>Academic Editor</role>
</contrib>
</contrib-group>
<aff id="af1-biomolecules-05-01122"><label>1</label>
Beijing Institute of Geriatrics, Xuanwu Hospital of Capital University of Medical Sciences, No.45 changchun St., Xicheng District, Beijing 100053, China; E-Mail:<email>xushngli_xw@163.com</email>
</aff>
<aff id="af2-biomolecules-05-01122"><label>2</label>
Parkinson’s disease Center of Beijing Institute for Brain Disorders, Beijing 100053, China</aff>
<author-notes><corresp id="c1-biomolecules-05-01122"><label>*</label>
Author to whom correspondence should be addressed; E-Mail: <email>pbchan90@gmail.com</email>
; Tel./Fax: +86-10-8316-1294.</corresp>
</author-notes>
<pub-date pub-type="epub"><day>05</day>
<month>6</month>
<year>2015</year>
</pub-date>
<pub-date pub-type="collection"><month>6</month>
<year>2015</year>
</pub-date>
<volume>5</volume>
<issue>2</issue>
<fpage>1122</fpage>
<lpage>1142</lpage>
<history><date date-type="received"><day>15</day>
<month>3</month>
<year>2015</year>
</date>
<date date-type="accepted"><day>29</day>
<month>4</month>
<year>2015</year>
</date>
</history>
<permissions><copyright-statement>© 2015 by the authors; licensee MDPI, Basel, Switzerland.</copyright-statement>
<copyright-year>2015</copyright-year>
<license><license-p><pmc-comment>CREATIVE COMMONS</pmc-comment>
This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/4.0/">http://creativecommons.org/licenses/by/4.0/</ext-link>
).</license-p>
</license>
</permissions>
<abstract><p>Parkinson’s disease (PD) is a very common neurodegenerative disorder characterized by the accumulation of α-synuclein (α-syn) into Lewy body (LB) inclusions and the loss of neuronmelanin (NM) containing dopamine (DA) neurons in the substantia nigra (SN). Pathological α-syn and NM are two prominent hallmarks in this selective and progressive neurodegenerative disease. Pathological α-syn can induce dopaminergic neuron death by various mechanisms, such as inducing oxidative stress and inhibiting protein degradation systems. Therefore, to explore the factors that trigger α-syn to convert from a non-toxic protein to toxic one is a pivotal question to clarify the mechanisms of PD pathogenesis. Many triggers for pathological α-syn aggregation have been identified, including missense mutations in the α-syn gene, higher concentration, and posttranslational modifications of α-Syn. Recently, the role of NM in inducing α-syn expression and aggregation has been suggested as a mechanism for this pigment to modulate neuronal vulnerability in PD. NM may be responsible for PD and age-associated increase and aggregation in α-syn. Here, we reviewed our previous study and other recent findings in the area of interaction between NM and α-syn.</p>
</abstract>
<kwd-group><kwd>alpha-synuclein</kwd>
<kwd>Parkinson’s disease</kwd>
<kwd>neuromelanin</kwd>
<kwd>oxidative stress</kwd>
</kwd-group>
</article-meta>
</front>
</pmc>
<affiliations><list><country><li>République populaire de Chine</li>
</country>
<settlement><li>Pékin</li>
</settlement>
</list>
<tree><country name="République populaire de Chine"><noRegion><name sortKey="Xu, Shengli" sort="Xu, Shengli" uniqKey="Xu S" first="Shengli" last="Xu">Shengli Xu</name>
</noRegion>
<name sortKey="Chan, Piu" sort="Chan, Piu" uniqKey="Chan P" first="Piu" last="Chan">Piu Chan</name>
</country>
</tree>
</affiliations>
</record>
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