Epigenetic Regulation of Fatty Acid Amide Hydrolase in Alzheimer Disease
Alzheimer disease (AD) is a progressive, degenerative and irreversible neurological disorder with few therapies available. In search for new potential targets, increasing evidence suggests a role for the endocannabinoid system (ECS) in the regulation of neurodegenerative processes. We have studied t...
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| Published in | PloS one Vol. 7; no. 6; p. e39186 |
|---|---|
| Main Authors | , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Public Library of Science
12.06.2012
Public Library of Science (PLoS) |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1932-6203 1932-6203 |
| DOI | 10.1371/journal.pone.0039186 |
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| Abstract | Alzheimer disease (AD) is a progressive, degenerative and irreversible neurological disorder with few therapies available. In search for new potential targets, increasing evidence suggests a role for the endocannabinoid system (ECS) in the regulation of neurodegenerative processes.
We have studied the gene expression status and the epigenetic regulation of ECS components in peripheral blood mononuclear cells (PBMCs) of subjects with late-onset AD (LOAD) and age-matched controls (CT).
We found an increase in fatty acid amide hydrolase (faah) gene expression in LOAD subjects (2.30 ± 0.48) when compared to CT (1.00 ± 0.14; *p<0.05) and no changes in the mRNA levels of any other gene of ECS elements. Consistently, we also observed in LOAD subjects an increase in FAAH protein levels (CT: 0.75 ± 0.04; LOAD: 1.11 ± 0.15; *p<0.05) and activity (pmol/min per mg protein CT: 103.80 ± 8.73; LOAD: 125.10 ± 4.00; *p<0.05), as well as a reduction in DNA methylation at faah gene promoter (CT: 55.90 ± 4.60%; LOAD: 41.20 ± 4.90%; *p<0.05).
Present findings suggest the involvement of FAAH in the pathogenesis of AD, highlighting the importance of epigenetic mechanisms in enzyme regulation; they also point to FAAH as a new potential biomarker for AD in easily accessible peripheral cells. |
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| AbstractList | Objective Alzheimer disease (AD) is a progressive, degenerative and irreversible neurological disorder with few therapies available. In search for new potential targets, increasing evidence suggests a role for the endocannabinoid system (ECS) in the regulation of neurodegenerative processes. Methods We have studied the gene expression status and the epigenetic regulation of ECS components in peripheral blood mononuclear cells (PBMCs) of subjects with late-onset AD (LOAD) and age-matched controls (CT). Results We found an increase in fatty acid amide hydrolase (faah) gene expression in LOAD subjects (2.30±0.48) when compared to CT (1.00±0.14; *p<0.05) and no changes in the mRNA levels of any other gene of ECS elements. Consistently, we also observed in LOAD subjects an increase in FAAH protein levels (CT: 0.75±0.04; LOAD: 1.11±0.15; *p<0.05) and activity (pmol/min per mg protein CT: 103.80±8.73; LOAD: 125.10±4.00; *p<0.05), as well as a reduction in DNA methylation at faah gene promoter (CT: 55.90±4.60%; LOAD: 41.20±4.90%; *p<0.05). Conclusions Present findings suggest the involvement of FAAH in the pathogenesis of AD, highlighting the importance of epigenetic mechanisms in enzyme regulation; they also point to FAAH as a new potential biomarker for AD in easily accessible peripheral cells. Objective Alzheimer disease (AD) is a progressive, degenerative and irreversible neurological disorder with few therapies available. In search for new potential targets, increasing evidence suggests a role for the endocannabinoid system (ECS) in the regulation of neurodegenerative processes. Methods We have studied the gene expression status and the epigenetic regulation of ECS components in peripheral blood mononuclear cells (PBMCs) of subjects with late-onset AD (LOAD) and age-matched controls (CT). Results We found an increase in fatty acid amide hydrolase (faah) gene expression in LOAD subjects (2.30±0.48) when compared to CT (1.00±0.14; *p<0.05) and no changes in the mRNA levels of any other gene of ECS elements. Consistently, we also observed in LOAD subjects an increase in FAAH protein levels (CT: 0.75±0.04; LOAD: 1.11±0.15; *p<0.05) and activity (pmol/min per mg protein CT: 103.80±8.73; LOAD: 125.10±4.00; *p<0.05), as well as a reduction in DNA methylation at faah gene promoter (CT: 55.90±4.60%; LOAD: 41.20±4.90%; *p<0.05). Conclusions Present findings suggest the involvement of FAAH in the pathogenesis of AD, highlighting the importance of epigenetic mechanisms in enzyme regulation; they also point to FAAH as a new potential biomarker for AD in easily accessible peripheral cells. Alzheimer disease (AD) is a progressive, degenerative and irreversible neurological disorder with few therapies available. In search for new potential targets, increasing evidence suggests a role for the endocannabinoid system (ECS) in the regulation of neurodegenerative processes. We have studied the gene expression status and the epigenetic regulation of ECS components in peripheral blood mononuclear cells (PBMCs) of subjects with late-onset AD (LOAD) and age-matched controls (CT). We found an increase in fatty acid amide hydrolase (faah) gene expression in LOAD subjects (2.30±0.48) when compared to CT (1.00±0.14; *p<0.05) and no changes in the mRNA levels of any other gene of ECS elements. Consistently, we also observed in LOAD subjects an increase in FAAH protein levels (CT: 0.75±0.04; LOAD: 1.11±0.15; *p<0.05) and activity (pmol/min per mg protein CT: 103.80±8.73; LOAD: 125.10±4.00; *p<0.05), as well as a reduction in DNA methylation at faah gene promoter (CT: 55.90±4.60%; LOAD: 41.20±4.90%; *p<0.05). Present findings suggest the involvement of FAAH in the pathogenesis of AD, highlighting the importance of epigenetic mechanisms in enzyme regulation; they also point to FAAH as a new potential biomarker for AD in easily accessible peripheral cells. Alzheimer disease (AD) is a progressive, degenerative and irreversible neurological disorder with few therapies available. In search for new potential targets, increasing evidence suggests a role for the endocannabinoid system (ECS) in the regulation of neurodegenerative processes.OBJECTIVEAlzheimer disease (AD) is a progressive, degenerative and irreversible neurological disorder with few therapies available. In search for new potential targets, increasing evidence suggests a role for the endocannabinoid system (ECS) in the regulation of neurodegenerative processes.We have studied the gene expression status and the epigenetic regulation of ECS components in peripheral blood mononuclear cells (PBMCs) of subjects with late-onset AD (LOAD) and age-matched controls (CT).METHODSWe have studied the gene expression status and the epigenetic regulation of ECS components in peripheral blood mononuclear cells (PBMCs) of subjects with late-onset AD (LOAD) and age-matched controls (CT).We found an increase in fatty acid amide hydrolase (faah) gene expression in LOAD subjects (2.30 ± 0.48) when compared to CT (1.00 ± 0.14; *p<0.05) and no changes in the mRNA levels of any other gene of ECS elements. Consistently, we also observed in LOAD subjects an increase in FAAH protein levels (CT: 0.75 ± 0.04; LOAD: 1.11 ± 0.15; *p<0.05) and activity (pmol/min per mg protein CT: 103.80 ± 8.73; LOAD: 125.10 ± 4.00; *p<0.05), as well as a reduction in DNA methylation at faah gene promoter (CT: 55.90 ± 4.60%; LOAD: 41.20 ± 4.90%; *p<0.05).RESULTSWe found an increase in fatty acid amide hydrolase (faah) gene expression in LOAD subjects (2.30 ± 0.48) when compared to CT (1.00 ± 0.14; *p<0.05) and no changes in the mRNA levels of any other gene of ECS elements. Consistently, we also observed in LOAD subjects an increase in FAAH protein levels (CT: 0.75 ± 0.04; LOAD: 1.11 ± 0.15; *p<0.05) and activity (pmol/min per mg protein CT: 103.80 ± 8.73; LOAD: 125.10 ± 4.00; *p<0.05), as well as a reduction in DNA methylation at faah gene promoter (CT: 55.90 ± 4.60%; LOAD: 41.20 ± 4.90%; *p<0.05).Present findings suggest the involvement of FAAH in the pathogenesis of AD, highlighting the importance of epigenetic mechanisms in enzyme regulation; they also point to FAAH as a new potential biomarker for AD in easily accessible peripheral cells.CONCLUSIONSPresent findings suggest the involvement of FAAH in the pathogenesis of AD, highlighting the importance of epigenetic mechanisms in enzyme regulation; they also point to FAAH as a new potential biomarker for AD in easily accessible peripheral cells. Alzheimer disease (AD) is a progressive, degenerative and irreversible neurological disorder with few therapies available. In search for new potential targets, increasing evidence suggests a role for the endocannabinoid system (ECS) in the regulation of neurodegenerative processes. We have studied the gene expression status and the epigenetic regulation of ECS components in peripheral blood mononuclear cells (PBMCs) of subjects with late-onset AD (LOAD) and age-matched controls (CT). We found an increase in fatty acid amide hydrolase (faah) gene expression in LOAD subjects (2.30 ± 0.48) when compared to CT (1.00 ± 0.14; *p<0.05) and no changes in the mRNA levels of any other gene of ECS elements. Consistently, we also observed in LOAD subjects an increase in FAAH protein levels (CT: 0.75 ± 0.04; LOAD: 1.11 ± 0.15; *p<0.05) and activity (pmol/min per mg protein CT: 103.80 ± 8.73; LOAD: 125.10 ± 4.00; *p<0.05), as well as a reduction in DNA methylation at faah gene promoter (CT: 55.90 ± 4.60%; LOAD: 41.20 ± 4.90%; *p<0.05). Present findings suggest the involvement of FAAH in the pathogenesis of AD, highlighting the importance of epigenetic mechanisms in enzyme regulation; they also point to FAAH as a new potential biomarker for AD in easily accessible peripheral cells. ObjectiveAlzheimer disease (AD) is a progressive, degenerative and irreversible neurological disorder with few therapies available. In search for new potential targets, increasing evidence suggests a role for the endocannabinoid system (ECS) in the regulation of neurodegenerative processes.MethodsWe have studied the gene expression status and the epigenetic regulation of ECS components in peripheral blood mononuclear cells (PBMCs) of subjects with late-onset AD (LOAD) and age-matched controls (CT).ResultsWe found an increase in fatty acid amide hydrolase (faah) gene expression in LOAD subjects (2.30 ± 0.48) when compared to CT (1.00 ± 0.14; *p<0.05) and no changes in the mRNA levels of any other gene of ECS elements. Consistently, we also observed in LOAD subjects an increase in FAAH protein levels (CT: 0.75 ± 0.04; LOAD: 1.11 ± 0.15; *p<0.05) and activity (pmol/min per mg protein CT: 103.80 ± 8.73; LOAD: 125.10 ± 4.00; *p<0.05), as well as a reduction in DNA methylation at faah gene promoter (CT: 55.90 ± 4.60%; LOAD: 41.20 ± 4.90%; *p<0.05).ConclusionsPresent findings suggest the involvement of FAAH in the pathogenesis of AD, highlighting the importance of epigenetic mechanisms in enzyme regulation; they also point to FAAH as a new potential biomarker for AD in easily accessible peripheral cells. |
| Audience | Academic |
| Author | Scarpini, Elio Altamura, A. Carlo Maccarrone, Mauro Di Francesco, Andrea Mari, Daniela Arosio, Beatrice D'Addario, Claudio Gussago, Cristina Dell'Osso, Bernardo Galimberti, Daniela Bari, Monica |
| AuthorAffiliation | 1 Department of Biomedical Sciences, University of Teramo, Teramo, Italy 4 Department of Neurological Sciences, “Dino Ferrari” Center, University of Milan, Fondazione Cà Granda, IRCCS Ospedale Maggiore Policlinico, Milan, Italy 3 Department of Psychiatry, University of Milan, Fondazione Cà Granda, IRCCS Ospedale Maggiore Policlinico, Milan, Italy 6 European Center for Brain Research (CERC)/IRCCS Santa Lucia Foundation, Rome, Italy 2 Geriatric Unit, Department of Medical Sciences and Community Health, University of Milan, Fondazione Cà Granda, IRCCS Ospedale Maggiore Policlinico, Milan, Italy 5 Department of Experimental Medicine and Biochemical Sciences, Tor Vergata University, Rome, Italy University of Kentucky, United States of America |
| AuthorAffiliation_xml | – name: 2 Geriatric Unit, Department of Medical Sciences and Community Health, University of Milan, Fondazione Cà Granda, IRCCS Ospedale Maggiore Policlinico, Milan, Italy – name: 6 European Center for Brain Research (CERC)/IRCCS Santa Lucia Foundation, Rome, Italy – name: University of Kentucky, United States of America – name: 3 Department of Psychiatry, University of Milan, Fondazione Cà Granda, IRCCS Ospedale Maggiore Policlinico, Milan, Italy – name: 5 Department of Experimental Medicine and Biochemical Sciences, Tor Vergata University, Rome, Italy – name: 1 Department of Biomedical Sciences, University of Teramo, Teramo, Italy – name: 4 Department of Neurological Sciences, “Dino Ferrari” Center, University of Milan, Fondazione Cà Granda, IRCCS Ospedale Maggiore Policlinico, Milan, Italy |
| Author_xml | – sequence: 1 givenname: Claudio surname: D'Addario fullname: D'Addario, Claudio – sequence: 2 givenname: Andrea surname: Di Francesco fullname: Di Francesco, Andrea – sequence: 3 givenname: Beatrice surname: Arosio fullname: Arosio, Beatrice – sequence: 4 givenname: Cristina surname: Gussago fullname: Gussago, Cristina – sequence: 5 givenname: Bernardo surname: Dell'Osso fullname: Dell'Osso, Bernardo – sequence: 6 givenname: Monica surname: Bari fullname: Bari, Monica – sequence: 7 givenname: Daniela surname: Galimberti fullname: Galimberti, Daniela – sequence: 8 givenname: Elio surname: Scarpini fullname: Scarpini, Elio – sequence: 9 givenname: A. Carlo surname: Altamura fullname: Altamura, A. Carlo – sequence: 10 givenname: Daniela surname: Mari fullname: Mari, Daniela – sequence: 11 givenname: Mauro surname: Maccarrone fullname: Maccarrone, Mauro |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/22720070$$D View this record in MEDLINE/PubMed |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Conceived and designed the experiments: CD MM. Performed the experiments: CD ADF BA CG BD DG MB. Analyzed the data: CD ADF BA BD DG MB. Contributed reagents/materials/analysis tools: CA DM ES MM. Wrote the paper: CD MM. |
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| Snippet | Alzheimer disease (AD) is a progressive, degenerative and irreversible neurological disorder with few therapies available. In search for new potential targets,... Objective Alzheimer disease (AD) is a progressive, degenerative and irreversible neurological disorder with few therapies available. In search for new... ObjectiveAlzheimer disease (AD) is a progressive, degenerative and irreversible neurological disorder with few therapies available. In search for new potential... Objective Alzheimer disease (AD) is a progressive, degenerative and irreversible neurological disorder with few therapies available. In search for new... |
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| SubjectTerms | Activities of daily living Advertising executives Aged Aging Alzheimer Disease - genetics Alzheimer's disease Amidohydrolases - genetics Base Sequence Biology Biomarkers Brain research Cannabinoids Cytochrome Deoxyribonucleic acid DNA DNA methylation DNA Primers Endocannabinoid system Epigenesis, Genetic Epigenetic inheritance Epigenetics Fatty acids Fatty-acid amide hydrolase Female Gene expression Genes Geriatrics Humans Hydrolase Hydrolases Leukocytes (mononuclear) Load matching Localization Male Medicine Memory Messenger RNA Metabolism Methylation Middle Aged Nervous system Neurodegeneration Neurodegenerative diseases Neurophysiology Pathogenesis Peripheral blood mononuclear cells Regulations |
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| Title | Epigenetic Regulation of Fatty Acid Amide Hydrolase in Alzheimer Disease |
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