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1. ESTUDIO CASOS-CONTROL DE MARCADORES DE ESTRÉS OXIDATIVO Y METABOLISMO DEL HIERRO PLASMÁTICO EN LA ENFERMEDAD DE PARKINSON

Author

Rosa Larumbe Ilundáin, Jose Vicente Ferrer Valls, José Javier Viñes Rueda, David Guerrero, and Pablo Fraile

Subjects
Medicine, Public aspects of medicine, RA1-1270
Abstract

Fundamento: Existe cada vez m s evidencia de la implicaci n de mecanismos de estr s oxidativo en la enfermedad de Parkinson. Se han descrito en la sustancia negra niveles menores de GSH, aumento del dep sito de hierro, aumento de los productos derivados de la peroxidaci n lip dica y alteraciones del complejo I mitocondrial. Sin embargo, son escasos los estudios de niveles de antioxidantes en sangre perif rica y de la influencia del consumo de nutrientes en el desarrollo de la enfermedad. M todos: Se estudia en un grupo de 79 pacientes con enfermedad de Parkinson idiop tica y en un grupo control de 107 sujetos, equiparados por edad, sexo y lugar de residencia, los niveles plasm ticos de: Glutati n reducido (GSH), Malonildialdeh do (MDA), cido rico, tocoferol, -caroteno, licopeno y diversos par metros del metabolismo del hierro. As mismo, se estima el consumo de ciertos antioxidantes a partir de una encuesta diet tica. Resultados: Hemos encontrado diferencias significativas (p 0,001) en los niveles plasm ticos de GSH entre casos (0,10 mol/ml 0,06) y controles (0,29 mol/ml 0,12). De igual modo, los niveles de cido rico en plasma fueron m s bajos (p 0,05) en los casos (4,96 mg/ml 1,96) que en los controles (5,39 mg/ml 1,13). No hemos encontrado diferencias significativas de los niveles plasm ticos de MDA, tocoferol, -caroteno y licopeno. Respecto al metabolismo del hierro, en los pacientes con EP encontramos valores de ferritina y de transferrina significativamente mayores que en los controles, con un ndice de saturaci n de la transferrina menor (p 0,05). El hierro no mostr cambios significativos entre casos y controles. Conclusiones: Los resultados de este estudio apoyan la posible implicaci n del estr s oxidativo en la patog nesis de la enfermedad de Parkinson y, a la vez, evidencian alteraciones de algunos par metros en sangre perif rica en concordancia con hallazgos conocidos en la sustancia negra.

Published
2001

2. Dementia Risk Score for a Population in Southern Europe Calculated Using Competing Risk Models

Author

Oliver Ibarrondo, José María Huerta, Pilar Amiano, María Encarnación Andreu-Reinón, Olatz Mokoroa, Eva Ardanaz, Rosa Larumbe, Sandra M. Colorado-Yohar, Fernando Navarro-Mateu, María Dolores Chirlaque, and Javier Mar

Subjects
Europe, Psychiatry and Mental health, Clinical Psychology, Risk Factors, Spain, Incidence, General Neuroscience, Humans, Dementia, General Medicine, Geriatrics and Gerontology
Abstract

Background: Dementia prevention can be addressed if the intervention is applied early. Objective: The objective of this study was to develop and validate competing risk models to predict the late risk of dementia based on variables assessed in middle age in a southern European population. Methods: We conducted a prospective observational study of the EPIC-Spain cohort that included 25,015 participants. Dementia cases were identified from electronic health records and validated by neurologists. Data were gathered on sociodemographic characteristics and cardiovascular risk factors. To stratify dementia risk, Fine and Gray competing risk prediction models were constructed for the entire sample and for over-55-year-olds. Risk scores were calculated for low (the 30% of the sample with the lowest risk), moderate (> 30% –60%), and high (> 60% –100%) risk. Results: The 755 cases of dementia identified represented a cumulative incidence of 3.1% throughout the study period. The AUC of the model for over-55-year-olds was much higher (80.8%) than the overall AUC (68.5%) in the first 15 years of follow-up and remained that way in the subsequent follow-up. The weight of the competing risk of death was greater than that of dementia and especially when the entire population was included. Conclusion: This study presents the first dementia risk score calculated in a southern European population in mid-life and followed up for 20 years. The score makes it feasible to achieve the early identification of individuals in a southern European population who could be targeted for the prevention of dementia based on the intensive control of risk factors.

Published
2022
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3. Incidence of Dementia and Associated Factors in the EPIC-Spain Dementia Cohort

Author

Rosa Larumbe, Mikel Tainta, José María Huerta, Diana Gavrila, Sandra Colorado-Yohar, Eva Ardanaz, María Dolores Chirlaque, Carmen Navarro, María Encarnación Andreu-Reinón, Javier Mar, Pilar Amiano, and Fernando Navarro-Mateu

Subjects
Adult, Male, medicine.medical_specialty, Alcohol Drinking, Hyperlipidemias, Cohort Studies, Epidemiology, Diabetes Mellitus, medicine, Humans, Dementia, Cumulative incidence, Prospective Studies, Aged, Aged, 80 and over, business.industry, Incidence, General Neuroscience, Medical record, Incidence (epidemiology), General Medicine, Middle Aged, medicine.disease, Confidence interval, Psychiatry and Mental health, Clinical Psychology, Spain, Cohort, Educational Status, Female, Geriatrics and Gerontology, business, Follow-Up Studies, Demography, Cohort study
Abstract

Background: Dementia has become a public health priority as the number of cases continues to grow worldwide. Objective: To assess dementia incidence and determinants in the EPIC-Spain Dementia Cohort. Methods: 25,015 participants (57% women) were recruited from three Spanish regions between 1992-1996 and followed-up for over 20 years. Incident cases were ascertained through individual revision of medical records of potential cases. Crude and age-adjusted incidence rates (IR) of dementia and sub-types (Alzheimer’s disease (AD), and non-AD) were calculated by sex. Neelson-Aalen cumulative incidence estimates at 10, 15, and 20 years were obtained for each sex and age group. Multivariate Royston-Parmar models were used to assess independent determinants. Results: Global IR were higher in women for dementia and AD, and similar by sex for non-AD. IR ranged from 0.09 cases of dementia (95% confidence interval: 0.06–0.13) and 0.05 (0.03–0.09) of AD per 1000 person-years (py) in participants below 60 years, to 23.2 (15.9–33.8) cases of dementia and 14.6 (9.1–33.5) of AD (per 1000 py) in those ≥85 years. Adjusted IR were consistently higher in women than men for overall dementia and AD. Up to 12.5% of women and 9.1% of men 60–65 years-old developed dementia within 20 years. Low education, diabetes, and hyperlipidemia were the main independent predictors of dementia risk, whereas alcohol showed an inverse association. Conclusion: Dementia incidence increased with age and was higher among women, but showed no geographical pattern. Dementia risk was higher among subjects with lower education, not drinking alcohol, and presenting cardiovascular risk factors.

Published
2020
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4. Progressive cognitive impairment and familial spastic paraparesis due to PRESENILIN 1 mutation: anatomoclinical characterization

Author

Miren Altuna, Rosa Larumbe, María Victoria Zelaya, Sira Moreno, Virginia García-Solaesa, Maite Mendioroz, María Antonia Ramos, and María Elena Erro

Subjects
Presenilin 1, Movement Disorders, Plaque, Amyloid, Cognitive impairment, Neurology, Paraparesis, Alzheimer Disease, Seizures, Mutation, Paraparesis, Spastic, Presenilin-1, Humans, Cognitive Dysfunction, Female, Neurology (clinical), Atrophy, Neuropathology, Autosomal dominant Alzheimer's disease
Abstract

Introduction Autosomal dominant Alzheimer's disease (ADAD) due to presenilin 1 (PSEN1) mutation can induce atypical neurological symptoms such as movement disorders and epileptic seizures in the context of early-onset progressive cognitive impairment. Methods This study includes the anatomoclinical description of three patients of two generations of the same family with movement disorders and progressive cognitive impairment. All were evaluated by trained neurologists, underwent protocolized neuropsychological evaluation, and were assessed by structural (magnetic resonance) and functional (SPECT, PET-18FDG, or PET-18F-Florbetapir) brain imaging tests. A molecular genetic study was performed for all patients, and post-mortem confirmatory anatomopathological evaluation for one of them. Results The three female patients had an age of onset of symptoms of 38-51 years. All developed progressive multidomain cognitive impairment, paraparesis, and dysarthria, two with ophthalmoparesis and one with untriggered epileptic seizures since early stages. Bilateral cortical fronto-parietal atrophy and global cortical hypoperfusion or posterior bilateral hypometabolism were detected. PET-18F-Florbetapir, when performed, was positive for amyloid cortical deposit. The molecular genetic study confirmed the PSEN1 mutation c.869-2 A>G. Postmortem study of one of them confirmed Alzheimer's disease anatomopathological features with classic cotton wool plaques (CWP), including coexistence of amyloid angiopathy and Lewy body co-pathology. Discussion The phenotype of ADAD due to PSEN1 mutations is very heterogeneous between and across the same family. Family history assessment should include information not only about cognitive decline, but also about movement disorders and untriggered epileptic seizures. Further studies are needed to identify genetic or epigenetic factors that determine phenotypic diversity in this disease.

Published
2021

5. Mediterranean Diet and Risk of Dementia and Alzheimer's Disease in the EPIC-Spain Dementia Cohort Study

Author

Eva Ardanaz, Diana Gavrila, Javier Mar, Mikel Tainta, Carmen Navarro, María Dolores Chirlaque, Pilar Amiano, Rosa Larumbe, José María Huerta, Sandra Colorado-Yohar, María Encarnación Andreu-Reinón, and Fernando Navarro-Mateu

Subjects
Adult, Male, medicine.medical_specialty, Mediterranean diet, lcsh:TX341-641, Lower risk, Diet, Mediterranean, Article, Cohort Studies, 03 medical and health sciences, 0302 clinical medicine, Alzheimer Disease, Risk Factors, Internal medicine, medicine, cohort study, Dementia, Humans, 030212 general & internal medicine, EPIC-Spain, Prospective cohort study, Aged, Nutrition and Dietetics, business.industry, prospective analysis, Incidence (epidemiology), Hazard ratio, Middle Aged, medicine.disease, European Prospective Investigation into Cancer and Nutrition, Spain, Case-Control Studies, Female, business, Alzheimer’s disease, lcsh:Nutrition. Foods and food supply, 030217 neurology & neurosurgery, Food Science, Cohort study
Abstract

The Mediterranean diet (MD) has shown to reduce the occurrence of several chronic diseases. To evaluate its potential protective role on dementia incidence we studied 16,160 healthy participants from the European Prospective Investigation into Cancer and Nutrition (EPIC)-Spain Dementia Cohort study recruited between 1992–1996 and followed up for a mean (±SD) of 21.6 (±3.4) years. A total of 459 incident cases of dementia were ascertained through expert revision of medical records. Data on habitual diet was collected through a validated diet history method to assess adherence to the relative Mediterranean Diet (rMED) score. Hazard ratios (HR) of dementia by rMED levels (low, medium and high adherence levels: ≤6, 7–10 and ≥11 points, respectively) were estimated using multivariable Cox models, whereas time-dependent effects were evaluated using flexible parametric Royston-Parmar (RP) models. Results of the fully adjusted model showed that high versus low adherence to the categorical rMED score was associated with a 20% (HR = 0.80, 95%CI: 0.60–1.06) lower risk of dementia overall and HR of dementia was 8% (HR = 0.92, 0.85–0.99, p = 0.021) lower for each 2-point increment of the continuous rMED score. By sub-types, a favorable association was also found in women for non-AD (HR per 2-points = 0.74, 95%CI: 0.62–0.89), while not statistically significant in men for AD (HR per 2-points = 0.88, 0.76–1.01). The association was stronger in participants with lower education. In conclusion, in this large prospective cohort study MD was inversely associated with dementia incidence after accounting for major cardiovascular risk factors. The results differed by dementia sub-type, sex, and education but there was no significant evidence of effect modification.

Published
2021

6. DNA methylation signature of human hippocampus in Alzheimer's disease is linked to neurogenesis

Author

Julie M. J. Lepesant, Carmen Echavarri, Ivonne Jericó, Miren Roldán, Idoia Blanco-Luquin, Iván Méndez-López, Rosa Larumbe, Luisa Di Stefano, Amaya Urdánoz-Casado, Miren Altuna, Álvaro Perdones, María Victoria Zelaya, Alberto Labarga, Maite Mendioroz, and Javier Sánchez-Ruiz de Gordoa

Subjects
0301 basic medicine, Adult, Male, Neurogenesis, Neurodevelopment, Hippocampus, tau Proteins, Biology, Hippocampal formation, Poised promoters, Adult neurogenesis, Epigenesis, Genetic, 03 medical and health sciences, 0302 clinical medicine, Alzheimer Disease, Genetics, Cadaver, Humans, Homeobox, Epigenetics, Phosphorylation, Promoter Regions, Genetic, Molecular Biology, Genetics (clinical), Aged, Oligonucleotide Array Sequence Analysis, Aged, 80 and over, DNA methylation, Research, Genes, Homeobox, Promoter, Methylation, Epigenome, Middle Aged, Cell biology, 030104 developmental biology, 030220 oncology & carcinogenesis, Case-Control Studies, Female, Alzheimer’s, Developmental Biology, Genome-Wide Association Study
Abstract

Background Drawing the epigenome landscape of Alzheimer’s disease (AD) still remains a challenge. To characterize the epigenetic molecular basis of the human hippocampus in AD, we profiled genome-wide DNA methylation levels in hippocampal samples from a cohort of pure AD patients and controls by using the Illumina 450K methylation arrays. Results Up to 118 AD-related differentially methylated positions (DMPs) were identified in the AD hippocampus, and extended mapping of specific regions was obtained by bisulfite cloning sequencing. AD-related DMPs were significantly correlated with phosphorylated tau burden. Functional analysis highlighted that AD-related DMPs were enriched in poised promoters that were not generally maintained in committed neural progenitor cells, as shown by ChiP-qPCR experiments. Interestingly, AD-related DMPs preferentially involved neurodevelopmental and neurogenesis-related genes. Finally, InterPro ontology analysis revealed enrichment in homeobox-containing transcription factors in the set of AD-related DMPs. Conclusions These results suggest that altered DNA methylation in the AD hippocampus occurs at specific regulatory regions crucial for neural differentiation supporting the notion that adult hippocampal neurogenesis may play a role in AD through epigenetic mechanisms. Graphical abstract Electronic supplementary material The online version of this article (10.1186/s13148-019-0672-7) contains supplementary material, which is available to authorized users.

Published
2019

7. ESTUDIO CASOS-CONTROL DE MARCADORES DE ESTRÉS OXIDATIVO Y METABOLISMO DEL HIERRO PLASMÁTICO EN LA ENFERMEDAD DE PARKINSON

Author

D. Guerrero, Jose Vicente Ferrer Valls, Rosa Larumbe Ilundáin, JJ Viñes Rueda, and Pablo Fraile

Subjects
Glutatión, business.industry, lcsh:Public aspects of medicine, lcsh:R, lcsh:Medicine, Nutritional status, Estrés oxidativo, lcsh:RA1-1270, General Medicine, Tocoferol, Iron blood, Ácido úrico, Enfermedad de Parkinson, Transferrina, Medicine, business, Humanities, Hierro
Abstract

Fundamento: Existe cada vez m s evidencia de la implicaci n de mecanismos de estr s oxidativo en la enfermedad de Parkinson. Se han descrito en la sustancia negra niveles menores de GSH, aumento del dep sito de hierro, aumento de los productos derivados de la peroxidaci n lip dica y alteraciones del complejo I mitocondrial. Sin embargo, son escasos los estudios de niveles de antioxidantes en sangre perif rica y de la influencia del consumo de nutrientes en el desarrollo de la enfermedad. M todos: Se estudia en un grupo de 79 pacientes con enfermedad de Parkinson idiop tica y en un grupo control de 107 sujetos, equiparados por edad, sexo y lugar de residencia, los niveles plasm ticos de: Glutati n reducido (GSH), Malonildialdeh do (MDA), cido rico, tocoferol, -caroteno, licopeno y diversos par metros del metabolismo del hierro. As mismo, se estima el consumo de ciertos antioxidantes a partir de una encuesta diet tica. Resultados: Hemos encontrado diferencias significativas (p 0,001) en los niveles plasm ticos de GSH entre casos (0,10 mol/ml 0,06) y controles (0,29 mol/ml 0,12). De igual modo, los niveles de cido rico en plasma fueron m s bajos (p 0,05) en los casos (4,96 mg/ml 1,96) que en los controles (5,39 mg/ml 1,13). No hemos encontrado diferencias significativas de los niveles plasm ticos de MDA, tocoferol, -caroteno y licopeno. Respecto al metabolismo del hierro, en los pacientes con EP encontramos valores de ferritina y de transferrina significativamente mayores que en los controles, con un ndice de saturaci n de la transferrina menor (p 0,05). El hierro no mostr cambios significativos entre casos y controles. Conclusiones: Los resultados de este estudio apoyan la posible implicaci n del estr s oxidativo en la patog nesis de la enfermedad de Parkinson y, a la vez, evidencian alteraciones de algunos par metros en sangre perif rica en concordancia con hallazgos conocidos en la sustancia negra.

Published
2001

8. Fourth meeting of the European Neurological Society 25–29 June 1994 Barcelona, Spain

Author

H. Hattig, C. Delli Pizzi, M. C. Addonizio, Michelle Davis, A. R. Giovagnoli, L. Florensa, M. Roth, J. de Kruijk, Francisco Lacruz, Ph. Dewailly, A. Toygar, C. Avendano, P.P. De Deyn, J. F. Hurtevent, F. Lomeila, T. W. Wong, Gordon T. Plant, M. Bud, H. J. Willison, DH Miller, D. W. Langdon, R. Cioni, J. Servan, A. Kaygisiz, E. Racadot, D. B. Schens, E. Picciola, L. Falip, C. Bouchard, J. Jotova, A. Jorge-Santamaria, P. Misra, A. Dufour, C. P. Panagopoulos, A. Venneri, B. Sredni, B. Angelard, M. Janelidze, M. Carreno, J. Obenberger, J. Pouget, H. W. Moser, R. Kaufmann, J. A. Molina, D. Linden, A. Martin Urda, E. Uvestad, A. Krone, J. P. Cochin, J. Mallecourt, A. Cambon-Thomsen, K. Violleau, P. Osschmann, A. M. Durocher, E. Bussaglia, D. M. Danielle, H. Efendi, C. Van Broeckhoven, K. G. Jordan, W. Rautenberg, C. Iniguez, J. M. Delgado, Graham Watson, M. Lawden, Gareth J. Barker, K. Stiasny, James T. Becker, G. Campanella, E. Peghi, A. Poli, A. Haddad, T. Yamawaki, Giacomo P. Comi, S. Sotgiu, B. Ersmark, A. Pomes, M. Ziegler, P. Ferrante, P. Ruppi, H. KuÇukoglu, R. Bouton, U. K. Rinne, P. Vieregge, M. Dary, P. Giunti, Peter J. Goadsby, S. Jung, E. Secor, A. Steinberg, N. Vila, M. A. Hernandez, M. Cursi, A. Enqelhardt, A. Engelhardt, J. Veitch, F. Di Silverio, F. Arnaud, B. Neundörfer, R. Brucher, Dominique Caparros-Lefebvre, B. Meyer, Marianne Dieterich, M. H. Snidaro, R. Gomez, R. Cerbo, M. Ragno, J. M. Vance, S. Nemni, A. Caliskan, F. Barros, I. Velcheva, D. Ceballos-Baumann, V. Barak, A. Avila, N. Antonova, F. Resche, S. Pappata, L. Varela, S. R. Silveira Santos, A. Cammarota, L. Naccache, Y. Nara, E. Tournier-Lasserves, R. Mobner, T. Chase, A. Ensenyat, J. Ulrich, G. Giegerich, M. Rother, M. Revilla, N. Nitschke, K. Honczarenko, E. Basart Tarrats, J. Blin, B. Jacob, J. Santamaria, S. Knezevic, J. L. Castillo, M. Antem, J. Colomer, O. Busse, Didier Hannequin, S. Carrier, J. B. Ruidavets, C. Rozman, J. Bogoussslavsky, J. Pascual Calvet, E. Monros, J. M. Polo, M. Zucconl, Javier Muruzabal, R. R. Allen, R. Rivolta, K. Haugaard, A. Nespolo, K. Hoang-Xuang, G. Bussone, T. Avramidis, E. Corsini, Christiana Franke, T. Vinogradova, H. Boot, K. Vestergaard, G. H. Jansen, N. Argentino, M. Raltzig, W. Linssen, Mark B. Pepys, P. Roblot, L. Lauritzen, E. Fainardi, D. Morin, T. X. Arbizu Urdiain, J. Wollenhaupt, S. Bostantjopoulou, G. Pavesi, A. D. Forman, Giovanni Fabbrini, D. Jean, J. J. Archelos, M. I. Blanchs, M. Del Gobbo, Anna Carla Turconi, Ch. Derouesné, Elio Scarpini, A. Visbeck, P. Castejon, J. P. Renou, F. Mounier-Vehier, G. Potagas, Ch. Duyckaerts, A. Filla, R. Schneider, G. Ronen, K. Nagata, J. P. Vedel, A. Henneberg, G. van Melle, C. Baratti, H. Knott, M. C. Prevett, A. Bes, B. Metin, Jos V. Reempts, L. Martorell, Mefkure Eraksoy, H. O. Handwerker, D. S. Younger, O. Oktem, D. Frongillo, C. Soriano-Soriano, L. Niehaus, F. Zipp, A. Tartaro, S Newman, R. H. Browne, P. Davous, R. Sanchez, M. Muros, M. E. Kornhuber, A. Lavarone, M. Mohr, M. R. Garcia, S. Russell, H. Kellar-Wood, M. R. Tola, B. Ostermeyer, Ch. Tzekov, K. Sartor, E. B. Ringelstein, P. P. Gazzaniga, Paul Krack, H. Fidaner, H. Rico, T. Dbaiss, F. Alameda, E. Torchiana, L. Rumbach, I. Charques, J. M. Bogaard, C. D. Frith, L. J. Rappelle, R. Brenner, A. Joutel, K. Fuxe, G. HÄcker, M. J. Blaser, J. Valls-SolÇ, G. Ulm, M. Alberdi, A. Bock, F. W. Bertelsmann, U. Wieshmann, J. Visa, J. R. Lupski, D. D'Amico, L. M. P. Ramos, A. A. Vanderbark, R. Horn, M. Warmuth, Dietmar Kühne, Mark S. Palmer, C. Ehrenheim, E. Canga, S. Viola, O. Scarpino, P. Naldi, R. Almeida, A. A. Raymond, J. Gamez, Stephan Arnold, A. DiGiovanni, J. Dalmau, C. C. Chari, H. F. Beer, J. C. Koetsier, J. Iriarte, E. Yunis, J. Casadevall, E. Le Guern, E. Stenager, S. R. Benbadis, J. M. Warter, F. Burklin, I. Theodorou, L. Johannesen, G. A. Graveland, X. Leclerc, I. Vecchio, L. Ozelius, G. Nicoletti, R. K. Gherardi, E. Esperet, M. L. Delodovici, F. Cattin, F. Paiau, Giorgio Sacilotto, C. A. J. Broere, D. Chavdarov, J. P. Willmer, C. H. Hawkes, Th. Naegele, E. Ellie, E. Dartigues, M. J. Guardiola, S. Hesse, Z. Levic, Marco Rovaris, P. Saugeir-Veber, B. A. Yaqub, H. F. Durwen, R. Larumbe, J. Ballabrina, M. Sendtner, J. Röther, M. Horstink, C. Kluglein, M.P. Montesi, H. Apaydin, J. Montoya, E. Waubant, Ch. Verellen-Dunoulin, A. Nicolai, J. Lopez-Delval, R. Lemon, G. Cantinho, E. Granieri, A. Zeviani, Wolfgang H. Oertel, U. Ficola, V. Di Piero, V. Fragola, K. Sabev, M. V. Guitera, I. Turki, F. Bolgert, P. Ingrand, J. M. Gobernado, L. M. E. Grimaldi, S. Baybas, B. Eymard, Y. Rolland, Y. Robitaille, Ta. Pampols, P. J. Koehler, A. Carroacedo, J. Vilchez, S. Di Vittorio, I. R. Rise, T. Nagy, M. Kuffner, E. Palazzini, A. Ott, J. Pruim, T. X. Arbizu, E. Manetti, C. Cervera, S. Felber, G. Gursoy, J. Scholz, G. A. Buscaino, M. S. Chen, A. Pascual, J. Hazan, J. U. Gajda, J. G. Cea, G. Bottini, G. Damalik, F. Le Doze, G. Bonaldi, J. M. Hew, C. Messina, A. M. Kennedy, J. M. Carney, N. M. F. Murray, M. Parent, M. Koepp, V. Dimova, D. De Leo, K. Jellinger, G. Salemi, S. Mientus, M. L. Hansen, F. Mazzucchelli, J. Vieth, M. Mauri, E. Bartels, L. Johannsen, C. Humphreys, J. Emile, D. N. Landon, E. Kansu, R. Sanchez-Pernaute, Rsj Frackowiak, M. Gonzalez Torres, L. Oller, C. Machedo, J. Kother, M. Billiard, H. Durak, T. Schindler, A. Frank, A. Uncini, A. Sbriccoli, C. Farinas, D. W. Paty, N. Fast, A. T. Zangaladze, A. Kerkhofs, J. M. Pino Garcia, I. De la Fuente, B. Marini, L. Gomez, I. Rubio, Alessandra Bardoni, C. Brodie, P. Acin, U. Sliwka, S. A. Hawkins, S. Tardieu, F. Vitullo, J. M. Pereira Monteino, R. Gagliardi, T. Jezewski, A. Cano, T. Lempert, F. Abad Alegria, G. Rotondo, D. Ince, C. Martinez Parra, Y. Huang, H. Luders, Y. Steinvil, F. G. A. Van Der Meche, R. Bianchi, A. Sanchez, T. Sevilla, J. M. Ketelslegers, A. Domzal-Stryga, M. Pandolfo, M. O. Josse, K. W. Neff, I. Blanco, G. W. Bruyn, O. W. Witte, J. L. Thibault, G. Andersen, J. Pariset, A. Marcone, R. J. M. Lane, A. Hofman, M. Verin, T. Matilla, P. Bedoucha, J. Roche, M. Lai, M. Collard, A. Ugarte, F. Gallecho, D. Silbersweig, C. Kennard, J. P. Azulay, T. W. Ho, P. L. I. Dellemijn, R. Girardello, F. Baas, B. Voss, F. Rozenberg, E. M. Brocker, V. Stanev, A. A. J. Soeterboek, A. Marra, A. Rey, E. Ertem, M. Sawradewicz-Rybak, J. De Keyser, P. Cavallari, F. Proust, Y. Chevalier, H. C. Hansen, D. Leys, C. A. Davie, K. Hoang-Xuan, C. Bairati, H. van Crevel, Thomas T. Warner, B. Bompais, A. Dobbeleir, T Campbell, C. Macko, C. J. M. Klijn, M. Dussallant, T. P. Berlit, W. Rozenbaum, M. J. van den Bent, W. A. Rocca, M. Muller, H. Hundemer, U. Zifko, M. Campera, F. Drislane, D. Ranoux, T. M. Kloss, Anil Kumar, I. Ruolt, C. Bargnani, B. Marescau, N. A. Losseff, S. Notermans, B. Kint, E. T. Burke, C. Aykut, J. Matias Guiu, P. Maquet, T. Drogendijk, M. Leone, K. von Ammon, M. Pepeliarska, C. Prados, L. DiGiamberardino, T. Logtenberg, G. Lenoir, I. Castaldo, Damhaut, M. Radionova, G. Sirabian, R. 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Brizioli, J. Calleja, L. Publio, M. Desi, R. Soffietti, P. Cortinovis-Tourniaire, E. F. Gonano, G. Cavaletti, S. Uselli, K. Westerlind, H. Betuel, C. O. Dhiver, H. Guggenheim, M. Hamon, R. Fazio, P. Lehikoinen, A. Esser, B. Sadzot, G. Fink, Angelo Antonini, D. Bendahan, V. Di Carlo, G. Galardi, A. F. Boller, M. Aksenova, Del Fiore, V. de la Sayette, H. Chabriat, A. Nicoletti, A. Dilouya, M. L. Harpin, E. Rouillet, J. Stam, A. Wolters, M. R. Delgado, Eduardo Tolosa, G. Said, A. J. Lees, L. Rinaldi, A. Schulze-Bonhage, MA Ron, C. Lefebvre, E. W. Radü, R. Alvarez, M. L. Bots, P. Reganati, S. Palazzi, A. Poggi, N. J. Scolding, V. Sazdovitch, T. Moreau, E. Maes, M. A. Estelies, P. Petkova, Jose-Felix Marti-Masso, G De La Meilleure, N. Mullatti, M. Rodegher, N. C. Notermans, T. A. T. Warner, S. Aktan, J. P. Louboutin, L. Volpe, C. Scheidt, W. Aust, C. M. Wiles, U. Schneider, S. K. Braekken, W. R. Willems, K. Usuku, Peter M. Rothwell, C. Talamon, M. L. Sacchetti, A. Codina, M. H. Marion, A. Santoro, J. Roda, A. Bordoni, D. J. Taylor, S. Ertas, H. H. Emmen, J. Vichez, V. BesanÇon, R. E. Passingham, M. L. Malosio, A. Vérier, M. Bamberg, A. W. Hansen, E. Mostacero, G. Gaudriault, Marie Vidailhet, B. Birebent, K. Strijckmans, F. Giannini, T. Kammer, I. Araujo, J. Nowicki, E. Nikolov, A. Hutzelmann, R. Gherardi, J. Verroust, L. Austoni, A. Scheller, A. Vazquez, S. Matheron, H. Holthausen, J. M. Gerard, M. Bataillard, S. Dethy, V. H. Patterson, V. Ivanez, N. P. Hirsch, F. Ozer, M. Sutter, C. Jacomet, M. Mora, Bruno Colombo, A. Sarropoulos, T. H. Papapetropoulos, M. Schwarz, D. S. Dinner, N. Acarin, B. Iandolo, J. O. Riis, P. R. J. Barnes, F. Taroni, J. Kazenwadel, L. Torre, A. Lugaresi, I. L. Henriques, S. Pauli, S. Alfonso, Pedro Quesada, A. S. T. Planting, J. M. Castilla, Thomas Gasser, M. Van der Linden, A. Alfaro, E. Nobile-Orazio, G. Popova, W. Vaalburg, F. G. A. van der Mech, L. Williams, F. Medina, J. P. Vernant, J. Yaouanq, B. Storch-Hagenlocher, A. Potemkowski, R. Riva, M. H. Mahagne, M. Ozturk, Ve. Drory, N. Konic, C. Jungreis, A. Pou Serradell, J. L. Gauvrit, G. J. Chelune, S. Hermandez, T. Dingus, L. Hewer, Ch. Koch, M. N. Metz-Lutz, G. Parlato, M. Sinaki, Charles Pierrot-Deseilligny, H. C. Diener, J. Broeckx, J. Weill-Fulazza, M. L. Villar, M. Rizzo, O. Ganslandt, C. Duran, N. A. Fletcher, G. Di Giovacchino, Susan T. Iannaccone, C. Kolig, N. Fabre, H. A. Crockard, Rita Bella, M. Tazir, E. Papagiannuli, K. Overgaard, Emma Ciafaloni, I. Lorenzetti, F. Viader, P. A. H. Millac, I. Montiel, L. H. Visser, M. Palomar, P. L. Murgia, H. Pedersen, Rafael Blesa, S. Seddigh, W. O. Renier, I. Lemahieu, H. M. L. Jansen, L. Rosin, J. Galofre, K. Mattos, M. Pondal, G. M. Hadjigeorgiou, D. Francis, L. Cantin, D. Stegeman, M. Rango, A. B. M. F. Karim, S. Schraff, B. Castellotti, I. Iriarte, E. Laborde, T. J. Tjan, R. Mutani, D. Toni, B. Bergaasco, J. G. Young, C. Klotzsch, A. Zincone, X. Ducrocq, M. Uchuya, O. J. Kolar, A. Quattrone, T. Bauermann, Nereo Bresolin, J. Vallée, B. C. Jacobs, A. Campos, Werner Poewe, J. A. Villanueva, A. W. Kornhuber, A. Malafosse, E. Diez-Tejedor, G. Jungreia, M. J. A. Puchner, A. Komiyama, O. Saribas, V. Volpini, L. Geremia, S. Bressi, A. Nibbio, Timothy E. Bates, T. z. Tzonev, E. Ideman, G. A. Damlacik, G. Martino, G. Crepaldi, T. Martino, Kjell Någren, E. Idiman, D. Samuel, J. M. Perez Trullen, Y. van der Graaf, J. O. Thorell, M. J. M. Dupuis, E. Sieber, R. D'Alessandro, C. Cazzaniga, J. Faiss, A. Tanguy, A. Schick, I. Hoksergen, A. Cardozo, R. Shakarishvili, G. K. Wennlng, J. L. Marti-Vilalta, J. Weissenbach, I. L. Simone, Amalia C. Bruni, Darius J. Adams, C. Weiller, A. Pietrangeli, F. Croria, C. Vigo-Pelfrey, Patricia Limousin, A. Ducros, G. Conti, O. Lindvall, E. Richter, M. Zuffi, A. Nappo, T. Riise, J. Wijdenes, M. J. Fernandez, J. Rosell, P. Vermersh, S. Servidei, M. S. C. Verdugo, F. Gouttiere, W. Solbach, M. Malbezin, I. S. Watanabe, A. Tumac, W. I. McDonald, D. A. Butterfield, P. P. Costa, F. deRino, F. Bamonti, J. M. Cesar, C. H. Lahoz, I. Mosely, M. Starck, M. H. Lemaitre, K. M. Stephan, S. Tex, R. Bokonjic, I. Mollee, L. Pastena, M. Gutierrez, F. Boiler, M. C. Martinez-Para, M. Velicogna, O. Obuz, A. Grinspan, M. Guarino, L. M. Cartier, E. Ruiz, D. Gambi, S. Messina, M. Villa, Michael G. Hanna, J. Valk, Leone Pascual, M. Clanet, Z. Argov, B. Ryniewicz, E. Magni, B. Berlanga, K. S. Wong, C. Gellera, C. Prevost, F. Gonzalez-Huix, R. Petraroli, J. E. G. Benedikz, I. Kojder, C. Bommelaer, L. Perusse, M. R. Bangioanni, Guy M. McKhann, A. Molina, C. Fresquet, E. Sindern, Florence Pasquier, M. J. Rosas, M. Altieri, O. Simoncini, M. Koutroumanidis, C. A. F. Tulleken, M. Dary-Auriol, S. Oueslati, H. Kruyer, I. Nishisho, C. R. Horning, A. Vital, G. V. Czettritz, J. Ph. Neau, B. Mihout, A. Ameri, M. Francis, S. Quasthoff, D. Taussig, S. Blunt, P. Valentin, C. Y. Gao, O. Heinzlef, H. d'Allens, C. Coudero, M. Erfas, G. Borghero, P. J. Modrego Pardo, M. C. Patrosso, N. L. Gershfeld, P. A. J. M. Boon, O. Sabouraud, M. Lara, J. Svennevig, G. L. Lenzi, A. Barrio, H. Villaroya, JosÇ M. Manubens, O. Boespflug-Tanguy, M. Carreras, D. A. Costiga, J. P. Breux, S. Lynn, C. Oliveras Ley, A. G. Herbaut, J. Nos, C. Tornali, Y. A. Hekster, J. L. Chopard, J. M. Manubens, P. Chemouilli, A. Jovicic, F. Dworzak, S. Smirne, S. E. Soudain, B. Gallano, D. Lubach, G. Masullo, G. Izquierdo, A. Pascual Leone Pascual, A. Sessa, V. Freitas, O. Crambes, L. Ouss, G. W. Van Dijk, P. Marchettini, P. Confalonieri, M. Donaghy, A. Munnich, M. Corbo, and M. E. L. van der Burg

Subjects
Neurology, business.industry, Media studies, Library science, Medicine, Neurology (clinical), business
Published
1994
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9. TREM2 upregulation correlates with 5-hydroxymethycytosine enrichment in Alzheimer’s disease hippocampus

Author

Naiara Celarain, Miren Roldán, Rosa Larumbe, Laura Pulido, Maite Mendioroz, Javier Sánchez-Ruiz de Gordoa, María Victoria Zelaya, and Carmen Echavarri

Subjects
Adult, Male, 0301 basic medicine, 5-Hydroxymethycytosine, Hippocampus, Biology, Cytosine, 03 medical and health sciences, 0302 clinical medicine, Alzheimer Disease, Gene expression, TREM2, Genetics, medicine, Humans, Epigenetics, Receptors, Immunologic, Molecular Biology, Genetics (clinical), Aged, Aged, 80 and over, Messenger RNA, DNA methylation, Membrane Glycoproteins, Research, Methylation, Middle Aged, medicine.disease, Molecular biology, Up-Regulation, 030104 developmental biology, 5-Methylcytosine, Female, Alzheimer's disease, Alzheimer’s disease, 030217 neurology & neurosurgery, Genome-Wide Association Study, Developmental Biology
Abstract

Background Recent genome-wide association studies revealed TREM2 rs75932628-T variant to be associated with Alzheimer’s disease (AD) and other neurodegenerative diseases. However, the role that TREM2 plays in sporadic AD is largely unknown. Our aim was to assess messenger RNA (mRNA) expression levels and DNA methylation profiling of TREM2 in human hippocampus in AD brain. We measured TREM2 mRNA levels in the hippocampus in a cohort of neuropathologically confirmed controls and pure AD cases showing no other protein deposits than β-amyloid and phosphorylated tau. We also examined DNA methylation levels in the TREM2 transcription start site (TSS)-associated region by bisulfite cloning sequencing and further extended the study by measuring 5-hydroxymethycytosine (5hmC) enrichment at different regions of TREM2 by 5hmC DNA immunoprecipitation combined with real-time qPCR. Results A 3.4-fold increase in TREM2 mRNA levels was observed in the hippocampus of AD cases compared to controls (p = 1.1E-05). Interestingly, TREM2 methylation was higher in AD cases compared to controls (76.2 % ± 15.5 versus 57.9 % ± 17.1; p = 0.0016). Moreover, TREM2 mRNA levels in the AD hippocampus correlated with enrichment in 5hmC at the TREM2 gene body (r = 0.771; p = 0.005). Conclusions TREM2 mRNA levels are increased in the human hippocampus in AD cases compared to controls. DNA methylation, and particularly 5hmC, may be involved in regulating TREM2 mRNA expression in the AD brain. Further studies are guaranteed to investigate in depth the role of 5hmC in AD and other neurodegenerative disorders. Electronic supplementary material The online version of this article (doi:10.1186/s13148-016-0202-9) contains supplementary material, which is available to authorized users.

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10. CRTC1 gene is differentially methylated in the human hippocampus in Alzheimer’s disease

Author

Iván Méndez, Rosa Larumbe, Carmen Echavarri, Miren Altuna, María Elena Erro, María Victoria Zelaya, Miren Roldán, Maite Mendioroz, Javier Sánchez-Ruiz de Gordoa, Naiara Celarain, and Idoya Rubio

Subjects
Adult, Male, 0301 basic medicine, medicine.medical_specialty, Pathology, Cognitive Neuroscience, Clinical Neurology, Hippocampus, tau Proteins, Biology, Epigenesis, Genetic, Young Adult, 03 medical and health sciences, 0302 clinical medicine, Alzheimer Disease, Internal medicine, medicine, Humans, RNA, Messenger, Epigenetics, Promoter Regions, Genetic, Gene, Transcription factor, Aged, Aged, 80 and over, DNA methylation, Research, Methylation, Middle Aged, medicine.disease, CRTC1, 030104 developmental biology, Endocrinology, CpG site, Neurology, Case-Control Studies, Female, Neurology (clinical), Alzheimer's disease, Alzheimer’s disease, 030217 neurology & neurosurgery, Transcription Factors
Abstract

Background CRTC1 (CREB regulated transcription coactivator 1) gene plays a role in synaptic plasticity, learning and long-term memory formation in the hippocampus. Recently, CRTC1 has been shown to be downregulated in Alzheimer’s disease (AD). Nevertheless, the mechanisms underlying CRTC1 dysregulation in AD remain unclear. Methods To understand better the epigenetic mechanisms regulating CRTC1 expression that may be altered in AD, we profiled DNA methylation at CpG site resolution by bisulfite cloning sequencing in two promoter regions (referred to as Prom1 and Prom2) of the CRTC1 gene in human hippocampus from controls and AD cases. Next, we correlated DNA methylation levels with AD-related pathology, i.e., β-amyloid and phosphorylated-tau (p-tau) burden and also measured CRTC1 mRNA levels by RT-qPCR. Results Methylation levels were lower in AD cases as compared to controls within both promoter regions (Prom1: 0.95 % vs. 5 %, p-value p-value CRTC1 methylation levels inversely correlated with AD-related neuropathological changes, particularly with p-tau deposition (rSpearman = -0.903, p CRTC1 mRNA levels was observed in hippocampus of AD cases compared to controls (p CRTC1 is downregulated in the AD hippocampus. Conclusions DNA methylation levels within two distinct promoter regions of the CRTC1 gene were decreased in human hippocampus affected by AD compared with controls and methylation within Prom1 showed a strong inverse correlation with p-tau deposition. Further studies are guaranteed to elucidate the precise role that CRTC1 methylation plays in AD pathophysiology.

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