Metabolomics‐based identification of metabolic alterations in PARK2
Objective Parkin is the causative gene for autosomal recessive familial Parkinson's disease (PD), although it remains unclear how parkin dysfunction is involved with the general condition. Recently, serum and/or plasma metabolomics revealed alterations in metabolic pathways that might reflect p...
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| Veröffentlicht in: | Annals of clinical and translational neurology 2019-03, Vol.6 (3), p.525-536 |
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| creator | Okuzumi, Ayami Hatano, Taku Ueno, Shin‐Ichi Ogawa, Takashi Saiki, Shinji Mori, Akio Koinuma, Takahiro Oji, Yutaka Ishikawa, Kei‐Ichi Fujimaki, Motoki Sato, Shigeto Ramamoorthy, Sivapriya Mohney, Robert P. Hattori, Nobutaka |
| description | Objective
Parkin is the causative gene for autosomal recessive familial Parkinson's disease (PD), although it remains unclear how parkin dysfunction is involved with the general condition. Recently, serum and/or plasma metabolomics revealed alterations in metabolic pathways that might reflect pathomechanisms of idiopathic PD (iPD). Thus, we hypothesized that serum metabolomics of patients with homozygous or compound heterozygous parkin mutations (namely, PARK2) might reflect metabolic alterations due to parkin dysfunction.
Methods
We enrolled 15 PARK2 patients (52 ± 17.6 years) confirmed with homozygous (seven cases) and compound heterozygous (eight cases) parkin mutations, along with 19 healthy age‐matched controls (51 ± 11.5 years). We analyzed 830 metabolites from participants’ serum using well‐established metabolomics technologies, including ultra‐high performance liquid chromatography/tandem mass spectroscopy.
Results
Based on metabolic profiles, hierarchical matrix analysis can divide samples between control and PARK2 subjects. Profiles from PARK2 patients showed significantly higher levels of fatty acid (FA) metabolites and oxidized lipids, and significantly lower levels of antioxidant, caffeine, and benzoate‐related metabolites.
Interpretation
Metabolomics can identify specific metabolic alterations in PARK2 patients compared with controls. Alterations in FA metabolites suggest a relationship between parkin function and lipid metabolism. The elevation of oxidized lipids in combination with decreasing antioxidants may reflect general hyperoxidative stress. Decreasing benzoate‐related metabolites might be due to the alteration in gut microbiota. Consequently, caffeine and its metabolites may be decreased due to malabsorption. These findings are similar to metabolic alterations in iPD. Thus, serum/plasma metabolomics may reflect the association between parkin dysfunction and parkinsonism. |
| doi_str_mv | 10.1002/acn3.724 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6414487</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2197888871</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5044-1d614e319889ebffdc2951a91df920a8060f666433e00258a183bd2d93a82cc43</originalsourceid><addsrcrecordid>eNp1kd1KwzAYhoMobsyBVyAFTzzpzF_b5EQYY_7g_EH0OKRpqhltM5tO2ZmX4DV6JaZuzimYk4QvDw_vxwvAPoIDBCE-lqoigwTTLdDFBLOQR5Bsb7w7oO_cFEKIEI5IgndBh0COUJTEXTC-0o1MbWFLo9zH23sqnc4Ck-mqMblRsjG2CmwelEvMqEAWja6_5i4wVXA7vLvEe2Anl4XT_dXdAw-n4_vReTi5ObsYDSehiiClIcpiRDVBnDGu0zzPFOYRkhxlOcdQMhjDPI5jSoj2i0VMIkbSDGecSIaVoqQHTpbe2TwtdaZ8yloWYlabUtYLYaURv38q8yQe7YuIKaKUJV5wtBLU9nmuXSNK45QuCllpO3cCI54wfxLk0cM_6NTO68qv11I-ng8If4Sqts7VOl-HQVC09Yi2HuHr8ejBZvg1-F2GB8Il8GoKvfhXJIaja9IKPwEaxpia</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2190252580</pqid></control><display><type>article</type><title>Metabolomics‐based identification of metabolic alterations in PARK2</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Wiley Online Library Journals Frontfile Complete</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Wiley-Blackwell Open Access Titles</source><source>PubMed Central</source><creator>Okuzumi, Ayami ; Hatano, Taku ; Ueno, Shin‐Ichi ; Ogawa, Takashi ; Saiki, Shinji ; Mori, Akio ; Koinuma, Takahiro ; Oji, Yutaka ; Ishikawa, Kei‐Ichi ; Fujimaki, Motoki ; Sato, Shigeto ; Ramamoorthy, Sivapriya ; Mohney, Robert P. ; Hattori, Nobutaka</creator><creatorcontrib>Okuzumi, Ayami ; Hatano, Taku ; Ueno, Shin‐Ichi ; Ogawa, Takashi ; Saiki, Shinji ; Mori, Akio ; Koinuma, Takahiro ; Oji, Yutaka ; Ishikawa, Kei‐Ichi ; Fujimaki, Motoki ; Sato, Shigeto ; Ramamoorthy, Sivapriya ; Mohney, Robert P. ; Hattori, Nobutaka</creatorcontrib><description>Objective
Parkin is the causative gene for autosomal recessive familial Parkinson's disease (PD), although it remains unclear how parkin dysfunction is involved with the general condition. Recently, serum and/or plasma metabolomics revealed alterations in metabolic pathways that might reflect pathomechanisms of idiopathic PD (iPD). Thus, we hypothesized that serum metabolomics of patients with homozygous or compound heterozygous parkin mutations (namely, PARK2) might reflect metabolic alterations due to parkin dysfunction.
Methods
We enrolled 15 PARK2 patients (52 ± 17.6 years) confirmed with homozygous (seven cases) and compound heterozygous (eight cases) parkin mutations, along with 19 healthy age‐matched controls (51 ± 11.5 years). We analyzed 830 metabolites from participants’ serum using well‐established metabolomics technologies, including ultra‐high performance liquid chromatography/tandem mass spectroscopy.
Results
Based on metabolic profiles, hierarchical matrix analysis can divide samples between control and PARK2 subjects. Profiles from PARK2 patients showed significantly higher levels of fatty acid (FA) metabolites and oxidized lipids, and significantly lower levels of antioxidant, caffeine, and benzoate‐related metabolites.
Interpretation
Metabolomics can identify specific metabolic alterations in PARK2 patients compared with controls. Alterations in FA metabolites suggest a relationship between parkin function and lipid metabolism. The elevation of oxidized lipids in combination with decreasing antioxidants may reflect general hyperoxidative stress. Decreasing benzoate‐related metabolites might be due to the alteration in gut microbiota. Consequently, caffeine and its metabolites may be decreased due to malabsorption. These findings are similar to metabolic alterations in iPD. Thus, serum/plasma metabolomics may reflect the association between parkin dysfunction and parkinsonism.</description><identifier>ISSN: 2328-9503</identifier><identifier>EISSN: 2328-9503</identifier><identifier>DOI: 10.1002/acn3.724</identifier><identifier>PMID: 30911576</identifier><language>eng</language><publisher>United States: John Wiley & Sons, Inc</publisher><subject>Adult ; Biomarkers - blood ; Caffeine ; Female ; Healthy Volunteers ; Humans ; Lipid Metabolism ; Lipids ; Male ; Metabolic Networks and Pathways ; Metabolism ; Metabolites ; Metabolome - genetics ; Metabolomics ; Middle Aged ; Mutation ; Parkinson's disease ; Parkinsonian Disorders - blood ; Parkinsonian Disorders - genetics ; Parkinsonian Disorders - metabolism ; Serum ; Ubiquitin-Protein Ligases - genetics ; Ubiquitin-Protein Ligases - metabolism</subject><ispartof>Annals of clinical and translational neurology, 2019-03, Vol.6 (3), p.525-536</ispartof><rights>2019 The Authors. published by Wiley Periodicals, Inc on behalf of American Neurological Association.</rights><rights>2019. This work is published under http://creativecommons.org/licenses/by-nc-nd/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5044-1d614e319889ebffdc2951a91df920a8060f666433e00258a183bd2d93a82cc43</citedby><cites>FETCH-LOGICAL-c5044-1d614e319889ebffdc2951a91df920a8060f666433e00258a183bd2d93a82cc43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6414487/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6414487/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,725,778,782,862,883,1414,11549,27911,27912,45561,45562,46039,46463,53778,53780</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30911576$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Okuzumi, Ayami</creatorcontrib><creatorcontrib>Hatano, Taku</creatorcontrib><creatorcontrib>Ueno, Shin‐Ichi</creatorcontrib><creatorcontrib>Ogawa, Takashi</creatorcontrib><creatorcontrib>Saiki, Shinji</creatorcontrib><creatorcontrib>Mori, Akio</creatorcontrib><creatorcontrib>Koinuma, Takahiro</creatorcontrib><creatorcontrib>Oji, Yutaka</creatorcontrib><creatorcontrib>Ishikawa, Kei‐Ichi</creatorcontrib><creatorcontrib>Fujimaki, Motoki</creatorcontrib><creatorcontrib>Sato, Shigeto</creatorcontrib><creatorcontrib>Ramamoorthy, Sivapriya</creatorcontrib><creatorcontrib>Mohney, Robert P.</creatorcontrib><creatorcontrib>Hattori, Nobutaka</creatorcontrib><title>Metabolomics‐based identification of metabolic alterations in PARK2</title><title>Annals of clinical and translational neurology</title><addtitle>Ann Clin Transl Neurol</addtitle><description>Objective
Parkin is the causative gene for autosomal recessive familial Parkinson's disease (PD), although it remains unclear how parkin dysfunction is involved with the general condition. Recently, serum and/or plasma metabolomics revealed alterations in metabolic pathways that might reflect pathomechanisms of idiopathic PD (iPD). Thus, we hypothesized that serum metabolomics of patients with homozygous or compound heterozygous parkin mutations (namely, PARK2) might reflect metabolic alterations due to parkin dysfunction.
Methods
We enrolled 15 PARK2 patients (52 ± 17.6 years) confirmed with homozygous (seven cases) and compound heterozygous (eight cases) parkin mutations, along with 19 healthy age‐matched controls (51 ± 11.5 years). We analyzed 830 metabolites from participants’ serum using well‐established metabolomics technologies, including ultra‐high performance liquid chromatography/tandem mass spectroscopy.
Results
Based on metabolic profiles, hierarchical matrix analysis can divide samples between control and PARK2 subjects. Profiles from PARK2 patients showed significantly higher levels of fatty acid (FA) metabolites and oxidized lipids, and significantly lower levels of antioxidant, caffeine, and benzoate‐related metabolites.
Interpretation
Metabolomics can identify specific metabolic alterations in PARK2 patients compared with controls. Alterations in FA metabolites suggest a relationship between parkin function and lipid metabolism. The elevation of oxidized lipids in combination with decreasing antioxidants may reflect general hyperoxidative stress. Decreasing benzoate‐related metabolites might be due to the alteration in gut microbiota. Consequently, caffeine and its metabolites may be decreased due to malabsorption. These findings are similar to metabolic alterations in iPD. Thus, serum/plasma metabolomics may reflect the association between parkin dysfunction and parkinsonism.</description><subject>Adult</subject><subject>Biomarkers - blood</subject><subject>Caffeine</subject><subject>Female</subject><subject>Healthy Volunteers</subject><subject>Humans</subject><subject>Lipid Metabolism</subject><subject>Lipids</subject><subject>Male</subject><subject>Metabolic Networks and Pathways</subject><subject>Metabolism</subject><subject>Metabolites</subject><subject>Metabolome - genetics</subject><subject>Metabolomics</subject><subject>Middle Aged</subject><subject>Mutation</subject><subject>Parkinson's disease</subject><subject>Parkinsonian Disorders - blood</subject><subject>Parkinsonian Disorders - genetics</subject><subject>Parkinsonian Disorders - metabolism</subject><subject>Serum</subject><subject>Ubiquitin-Protein Ligases - genetics</subject><subject>Ubiquitin-Protein Ligases - metabolism</subject><issn>2328-9503</issn><issn>2328-9503</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1kd1KwzAYhoMobsyBVyAFTzzpzF_b5EQYY_7g_EH0OKRpqhltM5tO2ZmX4DV6JaZuzimYk4QvDw_vxwvAPoIDBCE-lqoigwTTLdDFBLOQR5Bsb7w7oO_cFEKIEI5IgndBh0COUJTEXTC-0o1MbWFLo9zH23sqnc4Ck-mqMblRsjG2CmwelEvMqEAWja6_5i4wVXA7vLvEe2Anl4XT_dXdAw-n4_vReTi5ObsYDSehiiClIcpiRDVBnDGu0zzPFOYRkhxlOcdQMhjDPI5jSoj2i0VMIkbSDGecSIaVoqQHTpbe2TwtdaZ8yloWYlabUtYLYaURv38q8yQe7YuIKaKUJV5wtBLU9nmuXSNK45QuCllpO3cCI54wfxLk0cM_6NTO68qv11I-ng8If4Sqts7VOl-HQVC09Yi2HuHr8ejBZvg1-F2GB8Il8GoKvfhXJIaja9IKPwEaxpia</recordid><startdate>201903</startdate><enddate>201903</enddate><creator>Okuzumi, Ayami</creator><creator>Hatano, Taku</creator><creator>Ueno, Shin‐Ichi</creator><creator>Ogawa, Takashi</creator><creator>Saiki, Shinji</creator><creator>Mori, Akio</creator><creator>Koinuma, Takahiro</creator><creator>Oji, Yutaka</creator><creator>Ishikawa, Kei‐Ichi</creator><creator>Fujimaki, Motoki</creator><creator>Sato, Shigeto</creator><creator>Ramamoorthy, Sivapriya</creator><creator>Mohney, Robert P.</creator><creator>Hattori, Nobutaka</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88G</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>K9.</scope><scope>M0S</scope><scope>M2M</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201903</creationdate><title>Metabolomics‐based identification of metabolic alterations in PARK2</title><author>Okuzumi, Ayami ; Hatano, Taku ; Ueno, Shin‐Ichi ; Ogawa, Takashi ; Saiki, Shinji ; Mori, Akio ; Koinuma, Takahiro ; Oji, Yutaka ; Ishikawa, Kei‐Ichi ; Fujimaki, Motoki ; Sato, Shigeto ; Ramamoorthy, Sivapriya ; Mohney, Robert P. ; Hattori, Nobutaka</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5044-1d614e319889ebffdc2951a91df920a8060f666433e00258a183bd2d93a82cc43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Adult</topic><topic>Biomarkers - blood</topic><topic>Caffeine</topic><topic>Female</topic><topic>Healthy Volunteers</topic><topic>Humans</topic><topic>Lipid Metabolism</topic><topic>Lipids</topic><topic>Male</topic><topic>Metabolic Networks and Pathways</topic><topic>Metabolism</topic><topic>Metabolites</topic><topic>Metabolome - genetics</topic><topic>Metabolomics</topic><topic>Middle Aged</topic><topic>Mutation</topic><topic>Parkinson's disease</topic><topic>Parkinsonian Disorders - blood</topic><topic>Parkinsonian Disorders - genetics</topic><topic>Parkinsonian Disorders - metabolism</topic><topic>Serum</topic><topic>Ubiquitin-Protein Ligases - genetics</topic><topic>Ubiquitin-Protein Ligases - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Okuzumi, Ayami</creatorcontrib><creatorcontrib>Hatano, Taku</creatorcontrib><creatorcontrib>Ueno, Shin‐Ichi</creatorcontrib><creatorcontrib>Ogawa, Takashi</creatorcontrib><creatorcontrib>Saiki, Shinji</creatorcontrib><creatorcontrib>Mori, Akio</creatorcontrib><creatorcontrib>Koinuma, Takahiro</creatorcontrib><creatorcontrib>Oji, Yutaka</creatorcontrib><creatorcontrib>Ishikawa, Kei‐Ichi</creatorcontrib><creatorcontrib>Fujimaki, Motoki</creatorcontrib><creatorcontrib>Sato, Shigeto</creatorcontrib><creatorcontrib>Ramamoorthy, Sivapriya</creatorcontrib><creatorcontrib>Mohney, Robert P.</creatorcontrib><creatorcontrib>Hattori, Nobutaka</creatorcontrib><collection>Wiley-Blackwell Open Access Titles</collection><collection>Wiley Free Content</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Psychology Database (Alumni)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Psychology Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Annals of clinical and translational neurology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Okuzumi, Ayami</au><au>Hatano, Taku</au><au>Ueno, Shin‐Ichi</au><au>Ogawa, Takashi</au><au>Saiki, Shinji</au><au>Mori, Akio</au><au>Koinuma, Takahiro</au><au>Oji, Yutaka</au><au>Ishikawa, Kei‐Ichi</au><au>Fujimaki, Motoki</au><au>Sato, Shigeto</au><au>Ramamoorthy, Sivapriya</au><au>Mohney, Robert P.</au><au>Hattori, Nobutaka</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Metabolomics‐based identification of metabolic alterations in PARK2</atitle><jtitle>Annals of clinical and translational neurology</jtitle><addtitle>Ann Clin Transl Neurol</addtitle><date>2019-03</date><risdate>2019</risdate><volume>6</volume><issue>3</issue><spage>525</spage><epage>536</epage><pages>525-536</pages><issn>2328-9503</issn><eissn>2328-9503</eissn><abstract>Objective
Parkin is the causative gene for autosomal recessive familial Parkinson's disease (PD), although it remains unclear how parkin dysfunction is involved with the general condition. Recently, serum and/or plasma metabolomics revealed alterations in metabolic pathways that might reflect pathomechanisms of idiopathic PD (iPD). Thus, we hypothesized that serum metabolomics of patients with homozygous or compound heterozygous parkin mutations (namely, PARK2) might reflect metabolic alterations due to parkin dysfunction.
Methods
We enrolled 15 PARK2 patients (52 ± 17.6 years) confirmed with homozygous (seven cases) and compound heterozygous (eight cases) parkin mutations, along with 19 healthy age‐matched controls (51 ± 11.5 years). We analyzed 830 metabolites from participants’ serum using well‐established metabolomics technologies, including ultra‐high performance liquid chromatography/tandem mass spectroscopy.
Results
Based on metabolic profiles, hierarchical matrix analysis can divide samples between control and PARK2 subjects. Profiles from PARK2 patients showed significantly higher levels of fatty acid (FA) metabolites and oxidized lipids, and significantly lower levels of antioxidant, caffeine, and benzoate‐related metabolites.
Interpretation
Metabolomics can identify specific metabolic alterations in PARK2 patients compared with controls. Alterations in FA metabolites suggest a relationship between parkin function and lipid metabolism. The elevation of oxidized lipids in combination with decreasing antioxidants may reflect general hyperoxidative stress. Decreasing benzoate‐related metabolites might be due to the alteration in gut microbiota. Consequently, caffeine and its metabolites may be decreased due to malabsorption. These findings are similar to metabolic alterations in iPD. Thus, serum/plasma metabolomics may reflect the association between parkin dysfunction and parkinsonism.</abstract><cop>United States</cop><pub>John Wiley & Sons, Inc</pub><pmid>30911576</pmid><doi>10.1002/acn3.724</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Annals of clinical and translational neurology, 2019-03, Vol.6 (3), p.525-536 |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Wiley Online Library Journals Frontfile Complete; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Wiley-Blackwell Open Access Titles; PubMed Central |
| subjects | Adult Biomarkers - blood Caffeine Female Healthy Volunteers Humans Lipid Metabolism Lipids Male Metabolic Networks and Pathways Metabolism Metabolites Metabolome - genetics Metabolomics Middle Aged Mutation Parkinson's disease Parkinsonian Disorders - blood Parkinsonian Disorders - genetics Parkinsonian Disorders - metabolism Serum Ubiquitin-Protein Ligases - genetics Ubiquitin-Protein Ligases - metabolism |
| title | Metabolomics‐based identification of metabolic alterations in PARK2 |
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