Sex hormone-related neurosteroids differentially rescue bioenergetic deficits induced by amyloid-β or hyperphosphorylated tau protein.
Identifieur interne : 002437 ( PubMed/Corpus ); précédent : 002436; suivant : 002438Sex hormone-related neurosteroids differentially rescue bioenergetic deficits induced by amyloid-β or hyperphosphorylated tau protein.
Auteurs : Amandine Grimm ; Emily E. Biliouris ; Undine E. Lang ; Jürgen Götz ; Ayikoe Guy Mensah-Nyagan ; Anne EckertSource :
- Cellular and molecular life sciences : CMLS [ 1420-9071 ] ; 2016.
English descriptors
- KwdEn :
- Adenosine Triphosphate (metabolism), Alzheimer Disease (genetics), Alzheimer Disease (metabolism), Alzheimer Disease (pathology), Amyloid beta-Protein Precursor (genetics), Amyloid beta-Protein Precursor (metabolism), Cell Line, Energy Metabolism, Gonadal Steroid Hormones (metabolism), Humans, Membrane Potential, Mitochondrial, Neurons (metabolism), Neurons (pathology), Neurotransmitter Agents (metabolism), Phosphorylation, Point Mutation, Up-Regulation, tau Proteins (genetics), tau Proteins (metabolism).
- MESH :
- chemical , genetics : Amyloid beta-Protein Precursor, tau Proteins.
- chemical , metabolism : Adenosine Triphosphate, Amyloid beta-Protein Precursor, Gonadal Steroid Hormones, Neurotransmitter Agents, tau Proteins.
- genetics : Alzheimer Disease.
- metabolism : Alzheimer Disease, Neurons.
- pathology : Alzheimer Disease, Neurons.
- Cell Line, Energy Metabolism, Humans, Membrane Potential, Mitochondrial, Phosphorylation, Point Mutation, Up-Regulation.
Abstract
Alzheimer's disease (AD) is an age-related neurodegenerative disease marked by a progressive cognitive decline. Metabolic impairments are common hallmarks of AD, and amyloid-β (Aβ) peptide and hyperphosphorylated tau protein--the two foremost histopathological signs of AD--have been implicated in mitochondrial dysfunction. Neurosteroids have recently shown promise in alleviating cognitive and neuronal sequelae of AD. The present study evaluates the impact of neurosteroids belonging to the sex hormone family (progesterone, estradiol, estrone, testosterone, 3α-androstanediol) on mitochondrial dysfunction in cellular models of AD: human neuroblastoma cells (SH-SY5Y) stably transfected with constructs encoding (1) the human amyloid precursor protein (APP) resulting in overexpression of APP and Aβ, (2) wild-type tau (wtTau), and (3) mutant tau (P301L), that induces abnormal tau hyperphosphorylation. We show that while APP and P301L cells both display a drop in ATP levels, they present distinct mitochondrial impairments with regard to their bioenergetic profiles. The P301L cells presented a decreased maximal respiration and spare respiratory capacity, while APP cells exhibited, in addition, a decrease in basal respiration, ATP turnover, and glycolytic reserve. All neurosteroids showed beneficial effects on ATP production and mitochondrial membrane potential in APP/Aβ overexpressing cells while only progesterone and estradiol increased ATP levels in mutant tau cells. Of note, testosterone was more efficient in alleviating Aβ-induced mitochondrial deficits, while progesterone and estrogen were the most effective neurosteroids in our model of AD-related tauopathy. Our findings lend further support to the neuroprotective effects of neurosteroids in AD and may open new avenues for the development of gender-specific therapeutic approaches in AD.
DOI: 10.1007/s00018-015-1988-x
PubMed: 26198711
Links to Exploration step
pubmed:26198711Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Sex hormone-related neurosteroids differentially rescue bioenergetic deficits induced by amyloid-β or hyperphosphorylated tau protein.</title><author><name sortKey="Grimm, Amandine" sort="Grimm, Amandine" uniqKey="Grimm A" first="Amandine" last="Grimm">Amandine Grimm</name><affiliation><nlm:affiliation>Neurobiology Laboratory for Brain Aging and Mental Health, Transfaculty Research Platform, Molecular and Cognitive Neuroscience, University of Basel, Wilhelm Klein-Str. 27, 4012, Basel, Switzerland.</nlm:affiliation></affiliation></author><author><name sortKey="Biliouris, Emily E" sort="Biliouris, Emily E" uniqKey="Biliouris E" first="Emily E" last="Biliouris">Emily E. Biliouris</name><affiliation><nlm:affiliation>Neurobiology Laboratory for Brain Aging and Mental Health, Transfaculty Research Platform, Molecular and Cognitive Neuroscience, University of Basel, Wilhelm Klein-Str. 27, 4012, Basel, Switzerland.</nlm:affiliation></affiliation></author><author><name sortKey="Lang, Undine E" sort="Lang, Undine E" uniqKey="Lang U" first="Undine E" last="Lang">Undine E. Lang</name><affiliation><nlm:affiliation>Psychiatric University Clinics, University of Basel, Wilhelm Klein-Str. 27, 4012, Basel, Switzerland.</nlm:affiliation></affiliation></author><author><name sortKey="Gotz, Jurgen" sort="Gotz, Jurgen" uniqKey="Gotz J" first="Jürgen" last="Götz">Jürgen Götz</name><affiliation><nlm:affiliation>Clem Jones Centre for Ageing Dementia Research (CJCADR), Queensland Brain Institute (QBI), The University of Queensland, Brisbane, 4072, QLD, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Mensah Nyagan, Ayikoe Guy" sort="Mensah Nyagan, Ayikoe Guy" uniqKey="Mensah Nyagan A" first="Ayikoe Guy" last="Mensah-Nyagan">Ayikoe Guy Mensah-Nyagan</name><affiliation><nlm:affiliation>Biopathologie de la Myéline, Neuroprotection et Stratégies Thérapeutiques, INSERM U1119, Fédération de Médecine Translationnelle de Strasbourg (FMTS), Université de Strasbourg, Bâtiment 3 de la Faculté de Médecine, 11 rue Humann, 67 000, Strasbourg, France.</nlm:affiliation></affiliation></author><author><name sortKey="Eckert, Anne" sort="Eckert, Anne" uniqKey="Eckert A" first="Anne" last="Eckert">Anne Eckert</name><affiliation><nlm:affiliation>Neurobiology Laboratory for Brain Aging and Mental Health, Transfaculty Research Platform, Molecular and Cognitive Neuroscience, University of Basel, Wilhelm Klein-Str. 27, 4012, Basel, Switzerland. anne.eckert@upkbs.ch.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2016">2016</date><idno type="RBID">pubmed:26198711</idno><idno type="pmid">26198711</idno><idno type="doi">10.1007/s00018-015-1988-x</idno><idno type="wicri:Area/PubMed/Corpus">002437</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">002437</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Sex hormone-related neurosteroids differentially rescue bioenergetic deficits induced by amyloid-β or hyperphosphorylated tau protein.</title><author><name sortKey="Grimm, Amandine" sort="Grimm, Amandine" uniqKey="Grimm A" first="Amandine" last="Grimm">Amandine Grimm</name><affiliation><nlm:affiliation>Neurobiology Laboratory for Brain Aging and Mental Health, Transfaculty Research Platform, Molecular and Cognitive Neuroscience, University of Basel, Wilhelm Klein-Str. 27, 4012, Basel, Switzerland.</nlm:affiliation></affiliation></author><author><name sortKey="Biliouris, Emily E" sort="Biliouris, Emily E" uniqKey="Biliouris E" first="Emily E" last="Biliouris">Emily E. Biliouris</name><affiliation><nlm:affiliation>Neurobiology Laboratory for Brain Aging and Mental Health, Transfaculty Research Platform, Molecular and Cognitive Neuroscience, University of Basel, Wilhelm Klein-Str. 27, 4012, Basel, Switzerland.</nlm:affiliation></affiliation></author><author><name sortKey="Lang, Undine E" sort="Lang, Undine E" uniqKey="Lang U" first="Undine E" last="Lang">Undine E. Lang</name><affiliation><nlm:affiliation>Psychiatric University Clinics, University of Basel, Wilhelm Klein-Str. 27, 4012, Basel, Switzerland.</nlm:affiliation></affiliation></author><author><name sortKey="Gotz, Jurgen" sort="Gotz, Jurgen" uniqKey="Gotz J" first="Jürgen" last="Götz">Jürgen Götz</name><affiliation><nlm:affiliation>Clem Jones Centre for Ageing Dementia Research (CJCADR), Queensland Brain Institute (QBI), The University of Queensland, Brisbane, 4072, QLD, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Mensah Nyagan, Ayikoe Guy" sort="Mensah Nyagan, Ayikoe Guy" uniqKey="Mensah Nyagan A" first="Ayikoe Guy" last="Mensah-Nyagan">Ayikoe Guy Mensah-Nyagan</name><affiliation><nlm:affiliation>Biopathologie de la Myéline, Neuroprotection et Stratégies Thérapeutiques, INSERM U1119, Fédération de Médecine Translationnelle de Strasbourg (FMTS), Université de Strasbourg, Bâtiment 3 de la Faculté de Médecine, 11 rue Humann, 67 000, Strasbourg, France.</nlm:affiliation></affiliation></author><author><name sortKey="Eckert, Anne" sort="Eckert, Anne" uniqKey="Eckert A" first="Anne" last="Eckert">Anne Eckert</name><affiliation><nlm:affiliation>Neurobiology Laboratory for Brain Aging and Mental Health, Transfaculty Research Platform, Molecular and Cognitive Neuroscience, University of Basel, Wilhelm Klein-Str. 27, 4012, Basel, Switzerland. anne.eckert@upkbs.ch.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Cellular and molecular life sciences : CMLS</title><idno type="eISSN">1420-9071</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adenosine Triphosphate (metabolism)</term><term>Alzheimer Disease (genetics)</term><term>Alzheimer Disease (metabolism)</term><term>Alzheimer Disease (pathology)</term><term>Amyloid beta-Protein Precursor (genetics)</term><term>Amyloid beta-Protein Precursor (metabolism)</term><term>Cell Line</term><term>Energy Metabolism</term><term>Gonadal Steroid Hormones (metabolism)</term><term>Humans</term><term>Membrane Potential, Mitochondrial</term><term>Neurons (metabolism)</term><term>Neurons (pathology)</term><term>Neurotransmitter Agents (metabolism)</term><term>Phosphorylation</term><term>Point Mutation</term><term>Up-Regulation</term><term>tau Proteins (genetics)</term><term>tau Proteins (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Amyloid beta-Protein Precursor</term><term>tau Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Adenosine Triphosphate</term><term>Amyloid beta-Protein Precursor</term><term>Gonadal Steroid Hormones</term><term>Neurotransmitter Agents</term><term>tau Proteins</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Alzheimer Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Alzheimer Disease</term><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Alzheimer Disease</term><term>Neurons</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line</term><term>Energy Metabolism</term><term>Humans</term><term>Membrane Potential, Mitochondrial</term><term>Phosphorylation</term><term>Point Mutation</term><term>Up-Regulation</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Alzheimer's disease (AD) is an age-related neurodegenerative disease marked by a progressive cognitive decline. Metabolic impairments are common hallmarks of AD, and amyloid-β (Aβ) peptide and hyperphosphorylated tau protein--the two foremost histopathological signs of AD--have been implicated in mitochondrial dysfunction. Neurosteroids have recently shown promise in alleviating cognitive and neuronal sequelae of AD. The present study evaluates the impact of neurosteroids belonging to the sex hormone family (progesterone, estradiol, estrone, testosterone, 3α-androstanediol) on mitochondrial dysfunction in cellular models of AD: human neuroblastoma cells (SH-SY5Y) stably transfected with constructs encoding (1) the human amyloid precursor protein (APP) resulting in overexpression of APP and Aβ, (2) wild-type tau (wtTau), and (3) mutant tau (P301L), that induces abnormal tau hyperphosphorylation. We show that while APP and P301L cells both display a drop in ATP levels, they present distinct mitochondrial impairments with regard to their bioenergetic profiles. The P301L cells presented a decreased maximal respiration and spare respiratory capacity, while APP cells exhibited, in addition, a decrease in basal respiration, ATP turnover, and glycolytic reserve. All neurosteroids showed beneficial effects on ATP production and mitochondrial membrane potential in APP/Aβ overexpressing cells while only progesterone and estradiol increased ATP levels in mutant tau cells. Of note, testosterone was more efficient in alleviating Aβ-induced mitochondrial deficits, while progesterone and estrogen were the most effective neurosteroids in our model of AD-related tauopathy. Our findings lend further support to the neuroprotective effects of neurosteroids in AD and may open new avenues for the development of gender-specific therapeutic approaches in AD.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26198711</PMID><DateCreated><Year>2016</Year><Month>01</Month><Day>05</Day></DateCreated><DateCompleted><Year>2016</Year><Month>05</Month><Day>27</Day></DateCompleted><DateRevised><Year>2017</Year><Month>09</Month><Day>12</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1420-9071</ISSN><JournalIssue CitedMedium="Internet"><Volume>73</Volume><Issue>1</Issue><PubDate><Year>2016</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Cellular and molecular life sciences : CMLS</Title><ISOAbbreviation>Cell. Mol. Life Sci.</ISOAbbreviation></Journal><ArticleTitle>Sex hormone-related neurosteroids differentially rescue bioenergetic deficits induced by amyloid-β or hyperphosphorylated tau protein.</ArticleTitle><Pagination><MedlinePgn>201-15</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s00018-015-1988-x</ELocationID><Abstract><AbstractText>Alzheimer's disease (AD) is an age-related neurodegenerative disease marked by a progressive cognitive decline. Metabolic impairments are common hallmarks of AD, and amyloid-β (Aβ) peptide and hyperphosphorylated tau protein--the two foremost histopathological signs of AD--have been implicated in mitochondrial dysfunction. Neurosteroids have recently shown promise in alleviating cognitive and neuronal sequelae of AD. The present study evaluates the impact of neurosteroids belonging to the sex hormone family (progesterone, estradiol, estrone, testosterone, 3α-androstanediol) on mitochondrial dysfunction in cellular models of AD: human neuroblastoma cells (SH-SY5Y) stably transfected with constructs encoding (1) the human amyloid precursor protein (APP) resulting in overexpression of APP and Aβ, (2) wild-type tau (wtTau), and (3) mutant tau (P301L), that induces abnormal tau hyperphosphorylation. We show that while APP and P301L cells both display a drop in ATP levels, they present distinct mitochondrial impairments with regard to their bioenergetic profiles. The P301L cells presented a decreased maximal respiration and spare respiratory capacity, while APP cells exhibited, in addition, a decrease in basal respiration, ATP turnover, and glycolytic reserve. All neurosteroids showed beneficial effects on ATP production and mitochondrial membrane potential in APP/Aβ overexpressing cells while only progesterone and estradiol increased ATP levels in mutant tau cells. Of note, testosterone was more efficient in alleviating Aβ-induced mitochondrial deficits, while progesterone and estrogen were the most effective neurosteroids in our model of AD-related tauopathy. Our findings lend further support to the neuroprotective effects of neurosteroids in AD and may open new avenues for the development of gender-specific therapeutic approaches in AD.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Grimm</LastName><ForeName>Amandine</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Neurobiology Laboratory for Brain Aging and Mental Health, Transfaculty Research Platform, Molecular and Cognitive Neuroscience, University of Basel, Wilhelm Klein-Str. 27, 4012, Basel, Switzerland.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Psychiatric University Clinics, University of Basel, Wilhelm Klein-Str. 27, 4012, Basel, Switzerland.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Biopathologie de la Myéline, Neuroprotection et Stratégies Thérapeutiques, INSERM U1119, Fédération de Médecine Translationnelle de Strasbourg (FMTS), Université de Strasbourg, Bâtiment 3 de la Faculté de Médecine, 11 rue Humann, 67 000, Strasbourg, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Biliouris</LastName><ForeName>Emily E</ForeName><Initials>EE</Initials><AffiliationInfo><Affiliation>Neurobiology Laboratory for Brain Aging and Mental Health, Transfaculty Research Platform, Molecular and Cognitive Neuroscience, University of Basel, Wilhelm Klein-Str. 27, 4012, Basel, Switzerland.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Psychiatric University Clinics, University of Basel, Wilhelm Klein-Str. 27, 4012, Basel, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lang</LastName><ForeName>Undine E</ForeName><Initials>UE</Initials><AffiliationInfo><Affiliation>Psychiatric University Clinics, University of Basel, Wilhelm Klein-Str. 27, 4012, Basel, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Götz</LastName><ForeName>Jürgen</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Clem Jones Centre for Ageing Dementia Research (CJCADR), Queensland Brain Institute (QBI), The University of Queensland, Brisbane, 4072, QLD, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mensah-Nyagan</LastName><ForeName>Ayikoe Guy</ForeName><Initials>AG</Initials><AffiliationInfo><Affiliation>Biopathologie de la Myéline, Neuroprotection et Stratégies Thérapeutiques, INSERM U1119, Fédération de Médecine Translationnelle de Strasbourg (FMTS), Université de Strasbourg, Bâtiment 3 de la Faculté de Médecine, 11 rue Humann, 67 000, Strasbourg, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Eckert</LastName><ForeName>Anne</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Neurobiology Laboratory for Brain Aging and Mental Health, Transfaculty Research Platform, Molecular and Cognitive Neuroscience, University of Basel, Wilhelm Klein-Str. 27, 4012, Basel, Switzerland. anne.eckert@upkbs.ch.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Psychiatric University Clinics, University of Basel, Wilhelm Klein-Str. 27, 4012, Basel, Switzerland. anne.eckert@upkbs.ch.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>07</Month><Day>22</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Cell Mol Life Sci</MedlineTA><NlmUniqueID>9705402</NlmUniqueID><ISSNLinking>1420-682X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C545487">APP protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016564">Amyloid beta-Protein Precursor</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012739">Gonadal Steroid Hormones</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018377">Neurotransmitter Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016875">tau Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>8L70Q75FXE</RegistryNumber><NameOfSubstance UI="D000255">Adenosine Triphosphate</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Dis Colon Rectum. 2001 Apr;44(4):538-46; discussion 546-8</RefSource><PMID Version="1">11330581</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cell Mol Life Sci. 2008 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