Traumatic Brain Injury Alters the Metabolism and Facilitates Alzheimer’s Disease in a Murine Model
A majority of Alzheimer’s disease (AD) cases are sporadic without known cause. People who suffered from traumatic brain injury (TBI) are more likely to develop neurodegeneration and cognitive impairments. However, the role of TBI in pathophysiology of AD remains elusive. The present study intended t...
Gespeichert in:
| Veröffentlicht in: | Molecular neurobiology 2018-06, Vol.55 (6), p.4928-4939 |
|---|---|
| Hauptverfasser: | , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 4939 |
|---|---|
| container_issue | 6 |
| container_start_page | 4928 |
| container_title | Molecular neurobiology |
| container_volume | 55 |
| creator | Lou, Dandan Du, Yao Huang, Daochao Cai, Fang Zhang, Yun Li, Tinyu Zhou, Weihui Gao, Hongchang Song, Weihong |
| description | A majority of Alzheimer’s disease (AD) cases are sporadic without known cause. People who suffered from traumatic brain injury (TBI) are more likely to develop neurodegeneration and cognitive impairments. However, the role of TBI in pathophysiology of AD remains elusive. The present study intended to explore the effect of TBI on metabolism and its role in AD pathogenesis. We subjected double transgenic AD model mice APP23/PS45 to TBI. We found that TBI promoted β-secretase cleavage of amyloid β precursor protein and amyloid β protein deposition, and exuberated the cognitive impairments in AD mouse models.
1
H nuclear magnetic resonance (
1
H-NMR)-based metabolomics with multivariate analysis was performed to investigate the characteristic metabolites and the related metabolic pathways in the serum and urine samples of the mice. TBI affected the metabolic patterns, methylamine metabolism, and amino acid metabolism in serum samples. Urinary metabolites showed that glycolysis and the tricarboxylic acid (TCA) cycle were perturbed. The results indicate that TBI might facilitate Alzheimer’s pathogenesis by altering metabolism and inducing mitochondrial dysfunction. The study suggests that metabolite changes could also serve as biomarkers for TBI-induced neurodegeneration. |
| doi_str_mv | 10.1007/s12035-017-0687-z |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1926685423</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1926685423</sourcerecordid><originalsourceid>FETCH-LOGICAL-c438t-d80067477a5814c9096a1bf0b89a8ab4af00c4e56329086262774b07ddbcca083</originalsourceid><addsrcrecordid>eNp1kU1OHDEQha0IBJOBA2QTWWKTTYeyu9t2L2HIJEggNrC2qt01jEf9A3b3glnlGrleThKjISAhsapFfe_VUz3Gvgj4LgD0aRQS8jIDoTNQRmfbT2wmyrLKhDByj83AVHmmVWEO2ecYNwBSCtAH7FAarZVU5Yw1twGnDkfv-HlA3_PLfjOFJ37WjhQiH9fEr2nEemh97Dj2DV-i860fcaSYqO2afEfh7-8_kV_4SBiJJxfk11PwfRIPDbVHbH-FbaTjlzlnd8sft4tf2dXNz8vF2VXmityMWWMAlC60xtKIwlVQKRT1CmpTocG6wBWAK6hUuazApPxS66IG3TS1cwgmn7NvO9-HMDxOFEfb-eiobbGnYYpWVFIpUxYyT-jJO3QzTKFP6Wz6qc5TClCJEjvKhSHGQCv7EHyH4ckKsM8V2F0FNlVgnyuw26T5-uI81R01r4r_P0-A3AExrfp7Cm-nP3b9B_KIkXc</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2037347706</pqid></control><display><type>article</type><title>Traumatic Brain Injury Alters the Metabolism and Facilitates Alzheimer’s Disease in a Murine Model</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Lou, Dandan ; Du, Yao ; Huang, Daochao ; Cai, Fang ; Zhang, Yun ; Li, Tinyu ; Zhou, Weihui ; Gao, Hongchang ; Song, Weihong</creator><creatorcontrib>Lou, Dandan ; Du, Yao ; Huang, Daochao ; Cai, Fang ; Zhang, Yun ; Li, Tinyu ; Zhou, Weihui ; Gao, Hongchang ; Song, Weihong</creatorcontrib><description>A majority of Alzheimer’s disease (AD) cases are sporadic without known cause. People who suffered from traumatic brain injury (TBI) are more likely to develop neurodegeneration and cognitive impairments. However, the role of TBI in pathophysiology of AD remains elusive. The present study intended to explore the effect of TBI on metabolism and its role in AD pathogenesis. We subjected double transgenic AD model mice APP23/PS45 to TBI. We found that TBI promoted β-secretase cleavage of amyloid β precursor protein and amyloid β protein deposition, and exuberated the cognitive impairments in AD mouse models.
1
H nuclear magnetic resonance (
1
H-NMR)-based metabolomics with multivariate analysis was performed to investigate the characteristic metabolites and the related metabolic pathways in the serum and urine samples of the mice. TBI affected the metabolic patterns, methylamine metabolism, and amino acid metabolism in serum samples. Urinary metabolites showed that glycolysis and the tricarboxylic acid (TCA) cycle were perturbed. The results indicate that TBI might facilitate Alzheimer’s pathogenesis by altering metabolism and inducing mitochondrial dysfunction. The study suggests that metabolite changes could also serve as biomarkers for TBI-induced neurodegeneration.</description><identifier>ISSN: 0893-7648</identifier><identifier>EISSN: 1559-1182</identifier><identifier>DOI: 10.1007/s12035-017-0687-z</identifier><identifier>PMID: 28776265</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Alzheimer Disease - complications ; Alzheimer Disease - metabolism ; Alzheimer Disease - pathology ; Alzheimer's disease ; Amino acids ; Amyloid beta-Peptides - metabolism ; Amyloid precursor protein ; Animal models ; Animals ; Biomarkers ; Biomarkers - metabolism ; Biomedical and Life Sciences ; Biomedicine ; Brain ; Brain - metabolism ; Brain - pathology ; Brain Injuries, Traumatic - complications ; Brain Injuries, Traumatic - metabolism ; Brain Injuries, Traumatic - pathology ; Cell Biology ; Cognitive ability ; Disease Models, Animal ; Disease Progression ; Glycolysis ; Magnetic Resonance Spectroscopy ; Maze Learning - physiology ; Metabolic pathways ; Metabolism ; Metabolites ; Metabolomics ; Methylamine ; Mice ; Mice, Transgenic ; Mitochondria ; Multivariate analysis ; Neurobiology ; Neurodegeneration ; Neurology ; Neurosciences ; NMR ; Nuclear magnetic resonance ; Pathogenesis ; Secretase ; Transgenic mice ; Traumatic brain injury ; Tricarboxylic acid cycle ; Urine</subject><ispartof>Molecular neurobiology, 2018-06, Vol.55 (6), p.4928-4939</ispartof><rights>Springer Science+Business Media, LLC 2017</rights><rights>Molecular Neurobiology is a copyright of Springer, (2017). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c438t-d80067477a5814c9096a1bf0b89a8ab4af00c4e56329086262774b07ddbcca083</citedby><cites>FETCH-LOGICAL-c438t-d80067477a5814c9096a1bf0b89a8ab4af00c4e56329086262774b07ddbcca083</cites><orcidid>0000-0001-9928-889X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12035-017-0687-z$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12035-017-0687-z$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28776265$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lou, Dandan</creatorcontrib><creatorcontrib>Du, Yao</creatorcontrib><creatorcontrib>Huang, Daochao</creatorcontrib><creatorcontrib>Cai, Fang</creatorcontrib><creatorcontrib>Zhang, Yun</creatorcontrib><creatorcontrib>Li, Tinyu</creatorcontrib><creatorcontrib>Zhou, Weihui</creatorcontrib><creatorcontrib>Gao, Hongchang</creatorcontrib><creatorcontrib>Song, Weihong</creatorcontrib><title>Traumatic Brain Injury Alters the Metabolism and Facilitates Alzheimer’s Disease in a Murine Model</title><title>Molecular neurobiology</title><addtitle>Mol Neurobiol</addtitle><addtitle>Mol Neurobiol</addtitle><description>A majority of Alzheimer’s disease (AD) cases are sporadic without known cause. People who suffered from traumatic brain injury (TBI) are more likely to develop neurodegeneration and cognitive impairments. However, the role of TBI in pathophysiology of AD remains elusive. The present study intended to explore the effect of TBI on metabolism and its role in AD pathogenesis. We subjected double transgenic AD model mice APP23/PS45 to TBI. We found that TBI promoted β-secretase cleavage of amyloid β precursor protein and amyloid β protein deposition, and exuberated the cognitive impairments in AD mouse models.
1
H nuclear magnetic resonance (
1
H-NMR)-based metabolomics with multivariate analysis was performed to investigate the characteristic metabolites and the related metabolic pathways in the serum and urine samples of the mice. TBI affected the metabolic patterns, methylamine metabolism, and amino acid metabolism in serum samples. Urinary metabolites showed that glycolysis and the tricarboxylic acid (TCA) cycle were perturbed. The results indicate that TBI might facilitate Alzheimer’s pathogenesis by altering metabolism and inducing mitochondrial dysfunction. The study suggests that metabolite changes could also serve as biomarkers for TBI-induced neurodegeneration.</description><subject>Alzheimer Disease - complications</subject><subject>Alzheimer Disease - metabolism</subject><subject>Alzheimer Disease - pathology</subject><subject>Alzheimer's disease</subject><subject>Amino acids</subject><subject>Amyloid beta-Peptides - metabolism</subject><subject>Amyloid precursor protein</subject><subject>Animal models</subject><subject>Animals</subject><subject>Biomarkers</subject><subject>Biomarkers - metabolism</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brain</subject><subject>Brain - metabolism</subject><subject>Brain - pathology</subject><subject>Brain Injuries, Traumatic - complications</subject><subject>Brain Injuries, Traumatic - metabolism</subject><subject>Brain Injuries, Traumatic - pathology</subject><subject>Cell Biology</subject><subject>Cognitive ability</subject><subject>Disease Models, Animal</subject><subject>Disease Progression</subject><subject>Glycolysis</subject><subject>Magnetic Resonance Spectroscopy</subject><subject>Maze Learning - physiology</subject><subject>Metabolic pathways</subject><subject>Metabolism</subject><subject>Metabolites</subject><subject>Metabolomics</subject><subject>Methylamine</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Mitochondria</subject><subject>Multivariate analysis</subject><subject>Neurobiology</subject><subject>Neurodegeneration</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>NMR</subject><subject>Nuclear magnetic resonance</subject><subject>Pathogenesis</subject><subject>Secretase</subject><subject>Transgenic mice</subject><subject>Traumatic brain injury</subject><subject>Tricarboxylic acid cycle</subject><subject>Urine</subject><issn>0893-7648</issn><issn>1559-1182</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><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>eNp1kU1OHDEQha0IBJOBA2QTWWKTTYeyu9t2L2HIJEggNrC2qt01jEf9A3b3glnlGrleThKjISAhsapFfe_VUz3Gvgj4LgD0aRQS8jIDoTNQRmfbT2wmyrLKhDByj83AVHmmVWEO2ecYNwBSCtAH7FAarZVU5Yw1twGnDkfv-HlA3_PLfjOFJ37WjhQiH9fEr2nEemh97Dj2DV-i860fcaSYqO2afEfh7-8_kV_4SBiJJxfk11PwfRIPDbVHbH-FbaTjlzlnd8sft4tf2dXNz8vF2VXmityMWWMAlC60xtKIwlVQKRT1CmpTocG6wBWAK6hUuazApPxS66IG3TS1cwgmn7NvO9-HMDxOFEfb-eiobbGnYYpWVFIpUxYyT-jJO3QzTKFP6Wz6qc5TClCJEjvKhSHGQCv7EHyH4ckKsM8V2F0FNlVgnyuw26T5-uI81R01r4r_P0-A3AExrfp7Cm-nP3b9B_KIkXc</recordid><startdate>20180601</startdate><enddate>20180601</enddate><creator>Lou, Dandan</creator><creator>Du, Yao</creator><creator>Huang, Daochao</creator><creator>Cai, Fang</creator><creator>Zhang, Yun</creator><creator>Li, Tinyu</creator><creator>Zhou, Weihui</creator><creator>Gao, Hongchang</creator><creator>Song, Weihong</creator><general>Springer US</general><general>Springer Nature B.V</general><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>7QR</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88G</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-9928-889X</orcidid></search><sort><creationdate>20180601</creationdate><title>Traumatic Brain Injury Alters the Metabolism and Facilitates Alzheimer’s Disease in a Murine Model</title><author>Lou, Dandan ; Du, Yao ; Huang, Daochao ; Cai, Fang ; Zhang, Yun ; Li, Tinyu ; Zhou, Weihui ; Gao, Hongchang ; Song, Weihong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c438t-d80067477a5814c9096a1bf0b89a8ab4af00c4e56329086262774b07ddbcca083</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Alzheimer Disease - complications</topic><topic>Alzheimer Disease - metabolism</topic><topic>Alzheimer Disease - pathology</topic><topic>Alzheimer's disease</topic><topic>Amino acids</topic><topic>Amyloid beta-Peptides - metabolism</topic><topic>Amyloid precursor protein</topic><topic>Animal models</topic><topic>Animals</topic><topic>Biomarkers</topic><topic>Biomarkers - metabolism</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Brain</topic><topic>Brain - metabolism</topic><topic>Brain - pathology</topic><topic>Brain Injuries, Traumatic - complications</topic><topic>Brain Injuries, Traumatic - metabolism</topic><topic>Brain Injuries, Traumatic - pathology</topic><topic>Cell Biology</topic><topic>Cognitive ability</topic><topic>Disease Models, Animal</topic><topic>Disease Progression</topic><topic>Glycolysis</topic><topic>Magnetic Resonance Spectroscopy</topic><topic>Maze Learning - physiology</topic><topic>Metabolic pathways</topic><topic>Metabolism</topic><topic>Metabolites</topic><topic>Metabolomics</topic><topic>Methylamine</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>Mitochondria</topic><topic>Multivariate analysis</topic><topic>Neurobiology</topic><topic>Neurodegeneration</topic><topic>Neurology</topic><topic>Neurosciences</topic><topic>NMR</topic><topic>Nuclear magnetic resonance</topic><topic>Pathogenesis</topic><topic>Secretase</topic><topic>Transgenic mice</topic><topic>Traumatic brain injury</topic><topic>Tricarboxylic acid cycle</topic><topic>Urine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lou, Dandan</creatorcontrib><creatorcontrib>Du, Yao</creatorcontrib><creatorcontrib>Huang, Daochao</creatorcontrib><creatorcontrib>Cai, Fang</creatorcontrib><creatorcontrib>Zhang, Yun</creatorcontrib><creatorcontrib>Li, Tinyu</creatorcontrib><creatorcontrib>Zhou, Weihui</creatorcontrib><creatorcontrib>Gao, Hongchang</creatorcontrib><creatorcontrib>Song, Weihong</creatorcontrib><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>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Psychology Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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><jtitle>Molecular neurobiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lou, Dandan</au><au>Du, Yao</au><au>Huang, Daochao</au><au>Cai, Fang</au><au>Zhang, Yun</au><au>Li, Tinyu</au><au>Zhou, Weihui</au><au>Gao, Hongchang</au><au>Song, Weihong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Traumatic Brain Injury Alters the Metabolism and Facilitates Alzheimer’s Disease in a Murine Model</atitle><jtitle>Molecular neurobiology</jtitle><stitle>Mol Neurobiol</stitle><addtitle>Mol Neurobiol</addtitle><date>2018-06-01</date><risdate>2018</risdate><volume>55</volume><issue>6</issue><spage>4928</spage><epage>4939</epage><pages>4928-4939</pages><issn>0893-7648</issn><eissn>1559-1182</eissn><abstract>A majority of Alzheimer’s disease (AD) cases are sporadic without known cause. People who suffered from traumatic brain injury (TBI) are more likely to develop neurodegeneration and cognitive impairments. However, the role of TBI in pathophysiology of AD remains elusive. The present study intended to explore the effect of TBI on metabolism and its role in AD pathogenesis. We subjected double transgenic AD model mice APP23/PS45 to TBI. We found that TBI promoted β-secretase cleavage of amyloid β precursor protein and amyloid β protein deposition, and exuberated the cognitive impairments in AD mouse models.
1
H nuclear magnetic resonance (
1
H-NMR)-based metabolomics with multivariate analysis was performed to investigate the characteristic metabolites and the related metabolic pathways in the serum and urine samples of the mice. TBI affected the metabolic patterns, methylamine metabolism, and amino acid metabolism in serum samples. Urinary metabolites showed that glycolysis and the tricarboxylic acid (TCA) cycle were perturbed. The results indicate that TBI might facilitate Alzheimer’s pathogenesis by altering metabolism and inducing mitochondrial dysfunction. The study suggests that metabolite changes could also serve as biomarkers for TBI-induced neurodegeneration.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>28776265</pmid><doi>10.1007/s12035-017-0687-z</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0001-9928-889X</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0893-7648 |
| ispartof | Molecular neurobiology, 2018-06, Vol.55 (6), p.4928-4939 |
| issn | 0893-7648 1559-1182 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1926685423 |
| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Alzheimer Disease - complications Alzheimer Disease - metabolism Alzheimer Disease - pathology Alzheimer's disease Amino acids Amyloid beta-Peptides - metabolism Amyloid precursor protein Animal models Animals Biomarkers Biomarkers - metabolism Biomedical and Life Sciences Biomedicine Brain Brain - metabolism Brain - pathology Brain Injuries, Traumatic - complications Brain Injuries, Traumatic - metabolism Brain Injuries, Traumatic - pathology Cell Biology Cognitive ability Disease Models, Animal Disease Progression Glycolysis Magnetic Resonance Spectroscopy Maze Learning - physiology Metabolic pathways Metabolism Metabolites Metabolomics Methylamine Mice Mice, Transgenic Mitochondria Multivariate analysis Neurobiology Neurodegeneration Neurology Neurosciences NMR Nuclear magnetic resonance Pathogenesis Secretase Transgenic mice Traumatic brain injury Tricarboxylic acid cycle Urine |
| title | Traumatic Brain Injury Alters the Metabolism and Facilitates Alzheimer’s Disease in a Murine Model |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-07T21%3A58%3A32IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Traumatic%20Brain%20Injury%20Alters%20the%20Metabolism%20and%20Facilitates%20Alzheimer%E2%80%99s%20Disease%20in%20a%20Murine%20Model&rft.jtitle=Molecular%20neurobiology&rft.au=Lou,%20Dandan&rft.date=2018-06-01&rft.volume=55&rft.issue=6&rft.spage=4928&rft.epage=4939&rft.pages=4928-4939&rft.issn=0893-7648&rft.eissn=1559-1182&rft_id=info:doi/10.1007/s12035-017-0687-z&rft_dat=%3Cproquest_cross%3E1926685423%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2037347706&rft_id=info:pmid/28776265&rfr_iscdi=true |