Increasing membrane cholesterol of neurons in culture recapitulates Alzheimer's disease early phenotypes
It is suspected that excess of brain cholesterol plays a role in Alzheimer's disease (AD). Membrane-associated cholesterol was shown to be increased in the brain of individuals with sporadic AD and to correlate with the severity of the disease. We hypothesized that an increase of membrane chole...
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| Veröffentlicht in: | Molecular neurodegeneration 2014-12, Vol.9 (1), p.60-60, Article 60 |
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| creator | Marquer, Catherine Laine, Jeanne Dauphinot, Luce Hanbouch, Linda Lemercier-Neuillet, Camille Pierrot, Nathalie Bossers, Koen Le, Mickael Corlier, Fabian Benstaali, Caroline Saudou, Frédéric Thinakaran, Gopal Cartier, Nathalie Octave, Jean-Noël Duyckaerts, Charles Potier, Marie-Claude |
| description | It is suspected that excess of brain cholesterol plays a role in Alzheimer's disease (AD). Membrane-associated cholesterol was shown to be increased in the brain of individuals with sporadic AD and to correlate with the severity of the disease. We hypothesized that an increase of membrane cholesterol could trigger sporadic AD early phenotypes.
We thus acutely loaded the plasma membrane of cultured neurons with cholesterol to reach the 30% increase observed in AD brains. We found changes in gene expression profiles that are reminiscent of early AD stages. We also observed early AD cellular phenotypes. Indeed we found enlarged and aggregated early endosomes using confocal and electron microscopy after immunocytochemistry. In addition amyloid precursor protein vesicular transport was inhibited in neuronal processes, as seen by live-imaging. Finally transient membrane cholesterol loading lead to significantly increased amyloid-β42 secretion.
Membrane cholesterol increase in cultured neurons reproduces most early AD changes and could thus be a relevant model for deciphering AD mechanisms and identifying new therapeutic targets. |
| doi_str_mv | 10.1186/1750-1326-9-60 |
| format | Article |
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We thus acutely loaded the plasma membrane of cultured neurons with cholesterol to reach the 30% increase observed in AD brains. We found changes in gene expression profiles that are reminiscent of early AD stages. We also observed early AD cellular phenotypes. Indeed we found enlarged and aggregated early endosomes using confocal and electron microscopy after immunocytochemistry. In addition amyloid precursor protein vesicular transport was inhibited in neuronal processes, as seen by live-imaging. Finally transient membrane cholesterol loading lead to significantly increased amyloid-β42 secretion.
Membrane cholesterol increase in cultured neurons reproduces most early AD changes and could thus be a relevant model for deciphering AD mechanisms and identifying new therapeutic targets.</description><identifier>ISSN: 1750-1326</identifier><identifier>EISSN: 1750-1326</identifier><identifier>DOI: 10.1186/1750-1326-9-60</identifier><identifier>PMID: 25524049</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Advertising executives ; Alzheimer Disease - metabolism ; Alzheimer's disease ; Amyloid beta-Protein Precursor - metabolism ; Animals ; Apolipoproteins ; Binding sites ; Brain ; Cell Membrane - metabolism ; Cholesterol ; Cholesterol - metabolism ; Disease Models, Animal ; Gene expression ; Genes ; Genetic aspects ; Health aspects ; Lipids ; Memory - physiology ; Metabolism ; Microscopy ; Neurons ; Neurons - metabolism ; Neurosciences ; Ontology ; Pathology ; Phenotype ; Physiological aspects ; Proteins ; Rats, Sprague-Dawley ; Software ; Statistical analysis ; Target marketing ; Transcriptome</subject><ispartof>Molecular neurodegeneration, 2014-12, Vol.9 (1), p.60-60, Article 60</ispartof><rights>COPYRIGHT 2014 BioMed Central Ltd.</rights><rights>2014 Marquer et al.; licensee BioMed Central. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.</rights><rights>Marquer et al.; licensee BioMed Central. 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b642t-eb8902a39ff3766b642f6130395f2f5d266af4216fd45e742e6f8be3d8eab8d23</citedby><cites>FETCH-LOGICAL-b642t-eb8902a39ff3766b642f6130395f2f5d266af4216fd45e742e6f8be3d8eab8d23</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/PMC4280040/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4280040/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25524049$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Marquer, Catherine</creatorcontrib><creatorcontrib>Laine, Jeanne</creatorcontrib><creatorcontrib>Dauphinot, Luce</creatorcontrib><creatorcontrib>Hanbouch, Linda</creatorcontrib><creatorcontrib>Lemercier-Neuillet, Camille</creatorcontrib><creatorcontrib>Pierrot, Nathalie</creatorcontrib><creatorcontrib>Bossers, Koen</creatorcontrib><creatorcontrib>Le, Mickael</creatorcontrib><creatorcontrib>Corlier, Fabian</creatorcontrib><creatorcontrib>Benstaali, Caroline</creatorcontrib><creatorcontrib>Saudou, Frédéric</creatorcontrib><creatorcontrib>Thinakaran, Gopal</creatorcontrib><creatorcontrib>Cartier, Nathalie</creatorcontrib><creatorcontrib>Octave, Jean-Noël</creatorcontrib><creatorcontrib>Duyckaerts, Charles</creatorcontrib><creatorcontrib>Potier, Marie-Claude</creatorcontrib><title>Increasing membrane cholesterol of neurons in culture recapitulates Alzheimer's disease early phenotypes</title><title>Molecular neurodegeneration</title><addtitle>Mol Neurodegener</addtitle><description>It is suspected that excess of brain cholesterol plays a role in Alzheimer's disease (AD). Membrane-associated cholesterol was shown to be increased in the brain of individuals with sporadic AD and to correlate with the severity of the disease. We hypothesized that an increase of membrane cholesterol could trigger sporadic AD early phenotypes.
We thus acutely loaded the plasma membrane of cultured neurons with cholesterol to reach the 30% increase observed in AD brains. We found changes in gene expression profiles that are reminiscent of early AD stages. We also observed early AD cellular phenotypes. Indeed we found enlarged and aggregated early endosomes using confocal and electron microscopy after immunocytochemistry. In addition amyloid precursor protein vesicular transport was inhibited in neuronal processes, as seen by live-imaging. Finally transient membrane cholesterol loading lead to significantly increased amyloid-β42 secretion.
Membrane cholesterol increase in cultured neurons reproduces most early AD changes and could thus be a relevant model for deciphering AD mechanisms and identifying new therapeutic targets.</description><subject>Advertising executives</subject><subject>Alzheimer Disease - metabolism</subject><subject>Alzheimer's disease</subject><subject>Amyloid beta-Protein Precursor - metabolism</subject><subject>Animals</subject><subject>Apolipoproteins</subject><subject>Binding sites</subject><subject>Brain</subject><subject>Cell Membrane - metabolism</subject><subject>Cholesterol</subject><subject>Cholesterol - metabolism</subject><subject>Disease Models, Animal</subject><subject>Gene expression</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Lipids</subject><subject>Memory - physiology</subject><subject>Metabolism</subject><subject>Microscopy</subject><subject>Neurons</subject><subject>Neurons - metabolism</subject><subject>Neurosciences</subject><subject>Ontology</subject><subject>Pathology</subject><subject>Phenotype</subject><subject>Physiological aspects</subject><subject>Proteins</subject><subject>Rats, Sprague-Dawley</subject><subject>Software</subject><subject>Statistical analysis</subject><subject>Target marketing</subject><subject>Transcriptome</subject><issn>1750-1326</issn><issn>1750-1326</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqNkk1rFTEUhgdRbK1uXUrAhd1MzffMbIRLsVoouNF1yGRO7qRkkmsyU7j-ejO0XlutIFkknLx5OHmSqnpN8BkhrXxPGoFrwqisu1riJ9XxofD03vqoepHzNca8wVg8r46oEJRj3h1X42UwCXR2YYsmmPqkAyAzRg95hhQ9ihYFWFIMGbmAzOLnJQFKYPTOzYvXM2S08T9GcBOkdxkNLhccINDJ79FuhBDn_Q7yy-qZ1T7Dq7v5pPp28fHr-ef66suny_PNVd1LTuca-rbDVLPOWtZIuRatJAyzTlhqxUCl1JZTIu3ABTScgrRtD2xoQfftQNlJ9eGWu1v6CQYDYU7aq11yk057FbVTD3eCG9U23ihO2yIIF8DmFtC7-A_Awx0TJ7WaVqtp1Sm5Mk7vmkjx-1JUqsllA94Xu3HJisjyEoR3jfifKMFESrZS3_4RvY5LCsXmmsKiaRoif6e22oNywcbSpVmhaiM4lrzjjJfU2SOpMgaYnIkBrCv1xw6YFHNOYA9GSLl5-Yp_O3hz_yEO8V9_j_0EUWnaAg</recordid><startdate>20141218</startdate><enddate>20141218</enddate><creator>Marquer, Catherine</creator><creator>Laine, Jeanne</creator><creator>Dauphinot, Luce</creator><creator>Hanbouch, Linda</creator><creator>Lemercier-Neuillet, Camille</creator><creator>Pierrot, Nathalie</creator><creator>Bossers, Koen</creator><creator>Le, Mickael</creator><creator>Corlier, Fabian</creator><creator>Benstaali, Caroline</creator><creator>Saudou, Frédéric</creator><creator>Thinakaran, Gopal</creator><creator>Cartier, Nathalie</creator><creator>Octave, Jean-Noël</creator><creator>Duyckaerts, Charles</creator><creator>Potier, Marie-Claude</creator><general>BioMed Central Ltd</general><general>BioMed Central</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>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</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>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20141218</creationdate><title>Increasing membrane cholesterol of neurons in culture recapitulates Alzheimer's disease early phenotypes</title><author>Marquer, Catherine ; Laine, Jeanne ; Dauphinot, Luce ; Hanbouch, Linda ; Lemercier-Neuillet, Camille ; Pierrot, Nathalie ; Bossers, Koen ; Le, Mickael ; Corlier, Fabian ; Benstaali, Caroline ; Saudou, Frédéric ; Thinakaran, Gopal ; Cartier, Nathalie ; Octave, Jean-Noël ; Duyckaerts, Charles ; Potier, Marie-Claude</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b642t-eb8902a39ff3766b642f6130395f2f5d266af4216fd45e742e6f8be3d8eab8d23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Advertising executives</topic><topic>Alzheimer Disease - metabolism</topic><topic>Alzheimer's disease</topic><topic>Amyloid beta-Protein Precursor - metabolism</topic><topic>Animals</topic><topic>Apolipoproteins</topic><topic>Binding sites</topic><topic>Brain</topic><topic>Cell Membrane - metabolism</topic><topic>Cholesterol</topic><topic>Cholesterol - metabolism</topic><topic>Disease Models, Animal</topic><topic>Gene expression</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Lipids</topic><topic>Memory - physiology</topic><topic>Metabolism</topic><topic>Microscopy</topic><topic>Neurons</topic><topic>Neurons - metabolism</topic><topic>Neurosciences</topic><topic>Ontology</topic><topic>Pathology</topic><topic>Phenotype</topic><topic>Physiological aspects</topic><topic>Proteins</topic><topic>Rats, Sprague-Dawley</topic><topic>Software</topic><topic>Statistical analysis</topic><topic>Target marketing</topic><topic>Transcriptome</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Marquer, Catherine</creatorcontrib><creatorcontrib>Laine, Jeanne</creatorcontrib><creatorcontrib>Dauphinot, Luce</creatorcontrib><creatorcontrib>Hanbouch, Linda</creatorcontrib><creatorcontrib>Lemercier-Neuillet, Camille</creatorcontrib><creatorcontrib>Pierrot, Nathalie</creatorcontrib><creatorcontrib>Bossers, Koen</creatorcontrib><creatorcontrib>Le, Mickael</creatorcontrib><creatorcontrib>Corlier, Fabian</creatorcontrib><creatorcontrib>Benstaali, Caroline</creatorcontrib><creatorcontrib>Saudou, Frédéric</creatorcontrib><creatorcontrib>Thinakaran, Gopal</creatorcontrib><creatorcontrib>Cartier, Nathalie</creatorcontrib><creatorcontrib>Octave, Jean-Noël</creatorcontrib><creatorcontrib>Duyckaerts, Charles</creatorcontrib><creatorcontrib>Potier, Marie-Claude</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>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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 Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical 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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular neurodegeneration</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Marquer, Catherine</au><au>Laine, Jeanne</au><au>Dauphinot, Luce</au><au>Hanbouch, Linda</au><au>Lemercier-Neuillet, Camille</au><au>Pierrot, Nathalie</au><au>Bossers, Koen</au><au>Le, Mickael</au><au>Corlier, Fabian</au><au>Benstaali, Caroline</au><au>Saudou, Frédéric</au><au>Thinakaran, Gopal</au><au>Cartier, Nathalie</au><au>Octave, Jean-Noël</au><au>Duyckaerts, Charles</au><au>Potier, Marie-Claude</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Increasing membrane cholesterol of neurons in culture recapitulates Alzheimer's disease early phenotypes</atitle><jtitle>Molecular neurodegeneration</jtitle><addtitle>Mol Neurodegener</addtitle><date>2014-12-18</date><risdate>2014</risdate><volume>9</volume><issue>1</issue><spage>60</spage><epage>60</epage><pages>60-60</pages><artnum>60</artnum><issn>1750-1326</issn><eissn>1750-1326</eissn><abstract>It is suspected that excess of brain cholesterol plays a role in Alzheimer's disease (AD). Membrane-associated cholesterol was shown to be increased in the brain of individuals with sporadic AD and to correlate with the severity of the disease. We hypothesized that an increase of membrane cholesterol could trigger sporadic AD early phenotypes.
We thus acutely loaded the plasma membrane of cultured neurons with cholesterol to reach the 30% increase observed in AD brains. We found changes in gene expression profiles that are reminiscent of early AD stages. We also observed early AD cellular phenotypes. Indeed we found enlarged and aggregated early endosomes using confocal and electron microscopy after immunocytochemistry. In addition amyloid precursor protein vesicular transport was inhibited in neuronal processes, as seen by live-imaging. Finally transient membrane cholesterol loading lead to significantly increased amyloid-β42 secretion.
Membrane cholesterol increase in cultured neurons reproduces most early AD changes and could thus be a relevant model for deciphering AD mechanisms and identifying new therapeutic targets.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>25524049</pmid><doi>10.1186/1750-1326-9-60</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Advertising executives Alzheimer Disease - metabolism Alzheimer's disease Amyloid beta-Protein Precursor - metabolism Animals Apolipoproteins Binding sites Brain Cell Membrane - metabolism Cholesterol Cholesterol - metabolism Disease Models, Animal Gene expression Genes Genetic aspects Health aspects Lipids Memory - physiology Metabolism Microscopy Neurons Neurons - metabolism Neurosciences Ontology Pathology Phenotype Physiological aspects Proteins Rats, Sprague-Dawley Software Statistical analysis Target marketing Transcriptome |
| title | Increasing membrane cholesterol of neurons in culture recapitulates Alzheimer's disease early phenotypes |
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