Search

Your search keyword '"A. P. Sullivan"' showing total 106 results
Start Over Author "A. P. Sullivan" Journal molecular psychiatry
106 results on '"A. P. Sullivan"'

1. Genome-wide copy number variation association study in anorexia nervosa

Author

Walker, Alicia, Karlsson, Robert, Szatkiewicz, Jin P., Thornton, Laura M., Yilmaz, Zeynep, Leppä, Virpi M., Savva, Androula, Lin, Tian, Sidorenko, Julia, McRae, Allan, Kirov, George, Davies, Helena L., Fundín, Bengt T., Chawner, Samuel J. R. A., Song, Jie, Borg, Stina, Wen, Jia, Watson, Hunna J., Munn-Chernoff, Melissa A., Baker, Jessica H., Gordon, Scott, Berrettini, Wade H., Brandt, Harry, Crawford, Steven, Halmi, Katherine A., Kaplan, Allan S., Kaye, Walter H., Mitchell, James, Strober, Michael, Woodside, D. Blake, Pedersen, Nancy L., Parker, Richard, Jordan, Jennifer, Kennedy, Martin A., Birgegård, Andreas, Landén, Mikael, Martin, Nicholas G., Sullivan, Patrick F., Bulik, Cynthia M., and Wray, Naomi R.

Published
2024
Full Text
View/download PDF

3. Plasma proteins related to inflammatory diet predict future cognitive impairment

Author

Duggan, Michael R, Butler, Lauren, Peng, Zhongsheng, Daya, Gulzar N, Moghekar, Abhay, An, Yang, Rapp, Stephen R, Hayden, Kathleen M, Shadyab, Aladdin H, Natale, Ginny, Liu, Longjian, Snetselaar, Linda, Moaddel, Ruin, Rebholz, Casey M, Sullivan, Kevin, Ballantyne, Christie M, Resnick, Susan M, Ferrucci, Luigi, and Walker, Keenan A

Subjects
Biomedical and Clinical Sciences, Nutrition and Dietetics, Neurosciences, Neurodegenerative, Dementia, Acquired Cognitive Impairment, Brain Disorders, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Nutrition, Aging, Alzheimer's Disease, Clinical Research, Prevention, 2.1 Biological and endogenous factors, Aetiology, Detection, screening and diagnosis, 4.1 Discovery and preclinical testing of markers and technologies, Neurological, Inflammatory and immune system, Humans, Female, Aged, Proteomics, Alzheimer Disease, Cognitive Dysfunction, Diet, Blood Proteins, Biomarkers, tau Proteins, Amyloid beta-Peptides, Antigens, Neoplasm, Cell Adhesion Molecules, Biological Sciences, Medical and Health Sciences, Psychology and Cognitive Sciences, Psychiatry, Clinical sciences, Biological psychology, Clinical and health psychology
Abstract

Dysregulation of the immune system and dietary patterns that increase inflammation can increase the risk for cognitive decline, but the mechanisms by which inflammatory nutritional habits may affect the development of cognitive impairment in aging are not well understood. To determine whether plasma proteins linked to inflammatory diet predict future cognitive impairment, we applied high-throughput proteomic assays to plasma samples from a subset (n = 1528) of Women's Health Initiative Memory Study (WHIMS) participants (mean [SD] baseline age, 71.3 [SD 3.8] years). Results provide insights into how inflammatory nutritional patterns are associated with an immune-related proteome and identify a group of proteins (CXCL10, CCL3, HGF, OPG, CDCP1, NFATC3, ITGA11) related to future cognitive impairment over a 14-year follow-up period. Several of these inflammatory diet proteins were also associated with dementia risk across two external cohorts (ARIC, ESTHER), correlated with plasma biomarkers of Alzheimer's disease (AD) pathology (Aβ42/40) and/or neurodegeneration (NfL), and related to an MRI-defined index of neurodegenerative brain atrophy in a separate cohort (BLSA). In addition to evaluating their biological relevance, assessing their potential role in AD, and characterizing their immune-tissue/cell-specific expression, we leveraged published RNA-seq results to examine how the in vitro regulation of genes encoding these candidate proteins might be altered in response to an immune challenge. Our findings indicate how dietary patterns with higher inflammatory potential relate to plasma levels of immunologically relevant proteins and highlight the molecular mediators which predict subsequent risk for age-related cognitive impairment.

Published
2023

4. Investigating rare pathogenic/likely pathogenic exonic variation in bipolar disorder.

Author

Jia, Xiaoming, Goes, Fernando S, Locke, Adam E, Palmer, Duncan, Wang, Weiqing, Cohen-Woods, Sarah, Genovese, Giulio, Jackson, Anne U, Jiang, Chen, Kvale, Mark, Mullins, Niamh, Nguyen, Hoang, Pirooznia, Mehdi, Rivera, Margarita, Ruderfer, Douglas M, Shen, Ling, Thai, Khanh, Zawistowski, Matthew, Zhuang, Yongwen, Abecasis, Gonçalo, Akil, Huda, Bergen, Sarah, Burmeister, Margit, Chapman, Sinéad, DelaBastide, Melissa, Juréus, Anders, Kang, Hyun Min, Kwok, Pui-Yan, Li, Jun Z, Levy, Shawn E, Monson, Eric T, Moran, Jennifer, Sobell, Janet, Watson, Stanley, Willour, Virginia, Zöllner, Sebastian, Adolfsson, Rolf, Blackwood, Douglas, Boehnke, Michael, Breen, Gerome, Corvin, Aiden, Craddock, Nick, DiFlorio, Arianna, Hultman, Christina M, Landen, Mikael, Lewis, Cathryn, McCarroll, Steven A, Richard McCombie, W, McGuffin, Peter, McIntosh, Andrew, McQuillin, Andrew, Morris, Derek, Myers, Richard M, O'Donovan, Michael, Ophoff, Roel, Boks, Marco, Kahn, Rene, Ouwehand, Willem, Owen, Michael, Pato, Carlos, Pato, Michele, Posthuma, Danielle, Potash, James B, Reif, Andreas, Sklar, Pamela, Smoller, Jordan, Sullivan, Patrick F, Vincent, John, Walters, James, Neale, Benjamin, Purcell, Shaun, Risch, Neil, Schaefer, Catherine, Stahl, Eli A, Zandi, Peter P, and Scott, Laura J

Subjects
Humans, Genetic Predisposition to Disease, Bipolar Disorder, Schizophrenia, Polymorphism, Single Nucleotide, Genetic Variation, Genome-Wide Association Study, Exome, Brain Disorders, Prevention, Clinical Research, Human Genome, Serious Mental Illness, Genetics, Mental Health, 2.1 Biological and endogenous factors, Mental health, Biological Sciences, Medical and Health Sciences, Psychology and Cognitive Sciences, Psychiatry
Abstract

Bipolar disorder (BD) is a serious mental illness with substantial common variant heritability. However, the role of rare coding variation in BD is not well established. We examined the protein-coding (exonic) sequences of 3,987 unrelated individuals with BD and 5,322 controls of predominantly European ancestry across four cohorts from the Bipolar Sequencing Consortium (BSC). We assessed the burden of rare, protein-altering, single nucleotide variants classified as pathogenic or likely pathogenic (P-LP) both exome-wide and within several groups of genes with phenotypic or biologic plausibility in BD. While we observed an increased burden of rare coding P-LP variants within 165 genes identified as BD GWAS regions in 3,987 BD cases (meta-analysis OR = 1.9, 95% CI = 1.3-2.8, one-sided p = 6.0 × 10-4), this enrichment did not replicate in an additional 9,929 BD cases and 14,018 controls (OR = 0.9, one-side p = 0.70). Although BD shares common variant heritability with schizophrenia, in the BSC sample we did not observe a significant enrichment of P-LP variants in SCZ GWAS genes, in two classes of neuronal synaptic genes (RBFOX2 and FMRP) associated with SCZ or in loss-of-function intolerant genes. In this study, the largest analysis of exonic variation in BD, individuals with BD do not carry a replicable enrichment of rare P-LP variants across the exome or in any of several groups of genes with biologic plausibility. Moreover, despite a strong shared susceptibility between BD and SCZ through common genetic variation, we do not observe an association between BD risk and rare P-LP coding variants in genes known to modulate risk for SCZ.

Published
2021

5. Altered white matter microstructural organization in posttraumatic stress disorder across 3047 adults: results from the PGC-ENIGMA PTSD consortium

Author

Dennis, Emily L, Disner, Seth G, Fani, Negar, Salminen, Lauren E, Logue, Mark, Clarke, Emily K, Haswell, Courtney C, Averill, Christopher L, Baugh, Lee A, Bomyea, Jessica, Bruce, Steven E, Cha, Jiook, Choi, Kyle, Davenport, Nicholas D, Densmore, Maria, du Plessis, Stefan, Forster, Gina L, Frijling, Jessie L, Gonenc, Atilla, Gruber, Staci, Grupe, Daniel W, Guenette, Jeffrey P, Hayes, Jasmeet, Hofmann, David, Ipser, Jonathan, Jovanovic, Tanja, Kelly, Sinead, Kennis, Mitzy, Kinzel, Philipp, Koch, Saskia BJ, Koerte, Inga, Koopowitz, Sheri, Korgaonkar, Mayuresh, Krystal, John, Lebois, Lauren AM, Li, Gen, Magnotta, Vincent A, Manthey, Antje, May, Geoff J, Menefee, Deleene S, Nawijn, Laura, Nelson, Steven M, Neufeld, Richard WJ, Nitschke, Jack B, O’Doherty, Daniel, Peverill, Matthew, Ressler, Kerry J, Roos, Annerine, Sheridan, Margaret A, Sierk, Anika, Simmons, Alan, Simons, Raluca M, Simons, Jeffrey S, Stevens, Jennifer, Suarez-Jimenez, Benjamin, Sullivan, Danielle R, Théberge, Jean, Tran, Jana K, van den Heuvel, Leigh, van der Werff, Steven JA, van Rooij, Sanne JH, van Zuiden, Mirjam, Velez, Carmen, Verfaellie, Mieke, Vermeiren, Robert RJM, Wade, Benjamin SC, Wager, Tor, Walter, Henrik, Winternitz, Sherry, Wolff, Jonathan, York, Gerald, Zhu, Ye, Zhu, Xi, Abdallah, Chadi G, Bryant, Richard, Daniels, Judith K, Davidson, Richard J, Fercho, Kelene A, Franz, Carol, Geuze, Elbert, Gordon, Evan M, Kaufman, Milissa L, Kremen, William S, Lagopoulos, Jim, Lanius, Ruth A, Lyons, Michael J, McCauley, Stephen R, McGlinchey, Regina, McLaughlin, Katie A, Milberg, William, Neria, Yuval, Olff, Miranda, Seedat, Soraya, Shenton, Martha, Sponheim, Scott R, Stein, Dan J, Stein, Murray B, Straube, Thomas, Tate, David F, and van der Wee, Nic JA

Subjects
Biological Psychology, Psychology, Brain Disorders, Anxiety Disorders, Physical Injury - Accidents and Adverse Effects, Biomedical Imaging, Clinical Research, Mental Health, Post-Traumatic Stress Disorder (PTSD), Mental Illness, Neurosciences, Behavioral and Social Science, 2.1 Biological and endogenous factors, Mental health, Good Health and Well Being, Adolescent, Adult, Aged, Aged, 80 and over, Anisotropy, Brain, Diffusion Tensor Imaging, Female, Humans, Male, Middle Aged, Stress Disorders, Post-Traumatic, White Matter, Young Adult, Biological Sciences, Medical and Health Sciences, Psychology and Cognitive Sciences, Psychiatry, Clinical sciences, Biological psychology, Clinical and health psychology
Abstract

A growing number of studies have examined alterations in white matter organization in people with posttraumatic stress disorder (PTSD) using diffusion MRI (dMRI), but the results have been mixed which may be partially due to relatively small sample sizes among studies. Altered structural connectivity may be both a neurobiological vulnerability for, and a result of, PTSD. In an effort to find reliable effects, we present a multi-cohort analysis of dMRI metrics across 3047 individuals from 28 cohorts currently participating in the PGC-ENIGMA PTSD working group (a joint partnership between the Psychiatric Genomics Consortium and the Enhancing NeuroImaging Genetics through Meta-Analysis consortium). Comparing regional white matter metrics across the full brain in 1426 individuals with PTSD and 1621 controls (2174 males/873 females) between ages 18-83, 92% of whom were trauma-exposed, we report associations between PTSD and disrupted white matter organization measured by lower fractional anisotropy (FA) in the tapetum region of the corpus callosum (Cohen's d = -0.11, p = 0.0055). The tapetum connects the left and right hippocampus, for which structure and function have been consistently implicated in PTSD. Results were consistent even after accounting for the effects of multiple potentially confounding variables: childhood trauma exposure, comorbid depression, history of traumatic brain injury, current alcohol abuse or dependence, and current use of psychotropic medications. Our results show that PTSD may be associated with alterations in the broader hippocampal network.

Published
2021

6. Rare tandem repeat expansions associate with genes involved in synaptic and neuronal signaling functions in schizophrenia

Author

Wen, Jia, Trost, Brett, Engchuan, Worrawat, Halvorsen, Matthew, Pallotto, Linda M., Mitina, Aleksandra, Ancalade, NaEshia, Farrell, Martilias, Backstrom, Ian, Guo, Keyi, Pellecchia, Giovanna, Thiruvahindrapuram, Bhooma, Giusti-Rodriguez, Paola, Rosen, Jonathan David, Li, Yun, Won, Hyejung, Magnusson, Patrik K. E., Gyllensten, Ulf, Bassett, Anne S., Hultman, Christina M., Sullivan, Patrick F., Yuen, Ryan K. C., and Szatkiewicz, Jin P.

Published
2023
Full Text
View/download PDF

7. Contributions of common genetic variants to risk of schizophrenia among individuals of African and Latino ancestry

Author

Bigdeli, Tim B, Genovese, Giulio, Georgakopoulos, Penelope, Meyers, Jacquelyn L, Peterson, Roseann E, Iyegbe, Conrad O, Medeiros, Helena, Valderrama, Jorge, Achtyes, Eric D, Kotov, Roman, Stahl, Eli A, Abbott, Colony, Azevedo, Maria Helena, Belliveau, Richard A, Bevilacqua, Elizabeth, Bromet, Evelyn J, Byerley, William, Carvalho, Celia Barreto, Chapman, Sinéad B, DeLisi, Lynn E, Dumont, Ashley L, O’Dushlaine, Colm, Evgrafov, Oleg V, Fochtmann, Laura J, Gage, Diane, Kennedy, James L, Kinkead, Becky, Macedo, Antonio, Moran, Jennifer L, Morley, Christopher P, Dewan, Mantosh J, Nemesh, James, Perkins, Diana O, Purcell, Shaun M, Rakofsky, Jeffrey J, Scolnick, Edward M, Sklar, Brooke M, Sklar, Pamela, Smoller, Jordan W, Sullivan, Patrick F, Macciardi, Fabio, Marder, Stephen R, Gur, Ruben C, Gur, Raquel E, Braff, David L, Nicolini, Humberto, Escamilla, Michael A, Vawter, Marquis P, Sobell, Janet L, Malaspina, Dolores, Lehrer, Douglas S, Buckley, Peter F, Rapaport, Mark H, Knowles, James A, Fanous, Ayman H, Pato, Michele T, McCarroll, Steven A, and Pato, Carlos N

Subjects
Human Genome, Serious Mental Illness, Clinical Research, Schizophrenia, Brain Disorders, Genetics, Mental Health, Aetiology, 2.1 Biological and endogenous factors, Black People, Female, Genetic Loci, Genetic Predisposition to Disease, Genome-Wide Association Study, Hispanic or Latino, Humans, Male, Polymorphism, Single Nucleotide, Consortium on the Genetics of Schizophrenia (COGS) Investigators, Genomic Psychiatry Cohort (GPC) Consortium, Biological Sciences, Medical and Health Sciences, Psychology and Cognitive Sciences, Psychiatry
Abstract

Schizophrenia is a common, chronic and debilitating neuropsychiatric syndrome affecting tens of millions of individuals worldwide. While rare genetic variants play a role in the etiology of schizophrenia, most of the currently explained liability is within common variation, suggesting that variation predating the human diaspora out of Africa harbors a large fraction of the common variant attributable heritability. However, common variant association studies in schizophrenia have concentrated mainly on cohorts of European descent. We describe genome-wide association studies of 6152 cases and 3918 controls of admixed African ancestry, and of 1234 cases and 3090 controls of Latino ancestry, representing the largest such study in these populations to date. Combining results from the samples with African ancestry with summary statistics from the Psychiatric Genomics Consortium (PGC) study of schizophrenia yielded seven newly genome-wide significant loci, and we identified an additional eight loci by incorporating the results from samples with Latino ancestry. Leveraging population differences in patterns of linkage disequilibrium, we achieve improved fine-mapping resolution at 22 previously reported and 4 newly significant loci. Polygenic risk score profiling revealed improved prediction based on trans-ancestry meta-analysis results for admixed African (Nagelkerke's R2 = 0.032; liability R2 = 0.017; P

Published
2020

15. Genome-wide association study of panic disorder reveals genetic overlap with neuroticism and depression

Author

Forstner, Andreas J., Awasthi, Swapnil, Wolf, Christiane, Maron, Eduard, Erhardt, Angelika, Czamara, Darina, Eriksson, Elias, Lavebratt, Catharina, Allgulander, Christer, Friedrich, Nina, Becker, Jessica, Hecker, Julian, Rambau, Stefanie, Conrad, Rupert, Geiser, Franziska, McMahon, Francis J., Moebus, Susanne, Hess, Timo, Buerfent, Benedikt C., Hoffmann, Per, Herms, Stefan, Heilmann-Heimbach, Stefanie, Kockum, Ingrid, Olsson, Tomas, Alfredsson, Lars, Weber, Heike, Alpers, Georg W., Arolt, Volker, Fehm, Lydia, Fydrich, Thomas, Gerlach, Alexander L., Hamm, Alfons, Kircher, Tilo, Pané-Farré, Christiane A., Pauli, Paul, Rief, Winfried, Ströhle, Andreas, Plag, Jens, Lang, Thomas, Wittchen, Hans-Ulrich, Mattheisen, Manuel, Meier, Sandra, Metspalu, Andres, Domschke, Katharina, Reif, Andreas, Hovatta, Iiris, Lindefors, Nils, Andersson, Evelyn, Schalling, Martin, Mbarek, Hamdi, Milaneschi, Yuri, de Geus, Eco J. C., Boomsma, Dorret I., Penninx, Brenda W. J. H., Thorgeirsson, Thorgeir E., Steinberg, Stacy, Stefansson, Kari, Stefansson, Hreinn, Müller-Myhsok, Bertram, Hansen, Thomas Folkmann, Børglum, Anders D., Werge, Thomas, Mortensen, Preben Bo, Nordentoft, Merete, Hougaard, David M., Hultman, Christina M., Sullivan, Patrick F., Nöthen, Markus M., Woldbye, David P. D., Mors, Ole, Binder, Elisabeth B., Rück, Christian, Ripke, Stephan, Deckert, Jürgen, and Schumacher, Johannes

Published
2021
Full Text
View/download PDF

18. Evaluating historical candidate genes for schizophrenia

Author

Farrell, MS, Werge, T, Sklar, P, Owen, MJ, Ophoff, RA, O'Donovan, MC, Corvin, A, Cichon, S, and Sullivan, PF

Subjects
Human Genome, Brain Disorders, Mental Health, Schizophrenia, Genetics, Aetiology, 2.1 Biological and endogenous factors, Mental health, Genetic Predisposition to Disease, Genetic Variation, Genome-Wide Association Study, Genomics, Genotype, History, 20th Century, History, 21st Century, Humans, PubMed, Biological Sciences, Medical and Health Sciences, Psychology and Cognitive Sciences, Psychiatry
Abstract

Prior to the genome-wide association era, candidate gene studies were a major approach in schizophrenia genetics. In this invited review, we consider the current status of 25 historical candidate genes for schizophrenia (for example, COMT, DISC1, DTNBP1 and NRG1). The initial study for 24 of these genes explicitly evaluated common variant hypotheses about schizophrenia. Our evaluation included a meta-analysis of the candidate gene literature, incorporation of the results of the largest genomic study yet published for schizophrenia, ratings from informed researchers who have published on these genes, and ratings from 24 schizophrenia geneticists. On the basis of current empirical evidence and mostly consensual assessments of informed opinion, it appears that the historical candidate gene literature did not yield clear insights into the genetic basis of schizophrenia. A likely reason why historical candidate gene studies did not achieve their primary aims is inadequate statistical power. However, the considerable efforts embodied in these early studies unquestionably set the stage for current successes in genomic approaches to schizophrenia.

Published
2015

19. Polygenic dissection of diagnosis and clinical dimensions of bipolar disorder and schizophrenia

Author

Ruderfer, DM, Fanous, AH, Ripke, S, McQuillin, A, Amdur, RL, Gejman, PV, O'Donovan, MC, Andreassen, OA, Djurovic, S, Hultman, CM, Kelsoe, JR, Jamain, S, Landén, M, Leboyer, M, Nimgaonkar, V, Nurnberger, J, Smoller, JW, Craddock, N, Corvin, A, Sullivan, PF, Holmans, P, Sklar, P, and Kendler, KS

Subjects
Pharmacology and Pharmaceutical Sciences, Biomedical and Clinical Sciences, Brain Disorders, Serious Mental Illness, Genetics, Schizophrenia, Prevention, Mental Health, Bipolar Disorder, Human Genome, 2.1 Biological and endogenous factors, Aetiology, Mental health, Calcium Channels, L-Type, Case-Control Studies, Cell Cycle Proteins, Factor Analysis, Statistical, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Nuclear Proteins, Odds Ratio, Phenotype, Phosphatidylinositol 3-Kinases, Polymorphism, Single Nucleotide, Schizophrenic Psychology, bipolar, clinical symptoms, cross disorder, polygenic, schizophrenia, Schizophrenia Working Group of the Psychiatric Genomics Consortium, Bipolar Disorder Working Group of the Psychiatric Genomics Consortium, Cross-Disorder Working Group of the Psychiatric Genomics Consortium, Biological Sciences, Medical and Health Sciences, Psychology and Cognitive Sciences, Psychiatry, Clinical sciences, Biological psychology, Clinical and health psychology
Abstract

Bipolar disorder and schizophrenia are two often severe disorders with high heritabilities. Recent studies have demonstrated a large overlap of genetic risk loci between these disorders but diagnostic and molecular distinctions still remain. Here, we perform a combined genome-wide association study (GWAS) of 19 779 bipolar disorder (BP) and schizophrenia (SCZ) cases versus 19 423 controls, in addition to a direct comparison GWAS of 7129 SCZ cases versus 9252 BP cases. In our case-control analysis, we identify five previously identified regions reaching genome-wide significance (CACNA1C, IFI44L, MHC, TRANK1 and MAD1L1) and a novel locus near PIK3C2A. We create a polygenic risk score that is significantly different between BP and SCZ and show a significant correlation between a BP polygenic risk score and the clinical dimension of mania in SCZ patients. Our results indicate that first, combining diseases with similar genetic risk profiles improves power to detect shared risk loci and second, that future direct comparisons of BP and SCZ are likely to identify loci with significant differential effects. Identifying these loci should aid in the fundamental understanding of how these diseases differ biologically. These findings also indicate that combining clinical symptom dimensions and polygenic signatures could provide additional information that may someday be used clinically.

Published
2014

20. Genetics of response to cognitive behavior therapy in adults with major depression: a preliminary report

Author

Andersson, Evelyn, Crowley, James J., Lindefors, Nils, Ljótsson, Brjánn, Hedman-Lagerlöf, Erik, Boberg, Julia, El Alaoui, Samir, Karlsson, Robert, Lu, Yi, Mattheisen, Manuel, Kähler, Anna K., Svanborg, Cecilia, Mataix-Cols, David, Mattsson, Simon, Forsell, Erik, Kaldo, Viktor, Schalling, Martin, Lavebratt, Catharina, Sullivan, Patrick F., and Rück, Christian

Published
2019
Full Text
View/download PDF

21. Common-variant associations with fragile X syndrome

Author

Crowley, James J., Szatkiewicz, Jin, Kähler, Anna K., Giusti-Rodriguez, Paola, Ancalade, NaEshia, Booker, Jessica K., Carr, Jennifer L., Crawford, Greg E., Losh, Molly, Stockmeier, Craig A., Taylor, Annette K., Piven, Joseph, and Sullivan, Patrick F.

Published
2019
Full Text
View/download PDF

23. Correction: Investigating rare pathogenic/likely pathogenic exonic variation in bipolar disorder

Author

Jia, Xiaoming, Goes, Fernando S., Locke, Adam E., Palmer, Duncan, Wang, Weiqing, Cohen-Woods, Sarah, Genovese, Giulio, Jackson, Anne U., Jiang, Chen, Kvale, Mark, Mullins, Niamh, Nguyen, Hoang, Pirooznia, Mehdi, Rivera, Margarita, Ruderfer, Douglas M., Shen, Ling, Thai, Khanh, Zawistowski, Matthew, Zhuang, Yongwen, Abecasis, Gonçalo, Akil, Huda, Bergen, Sarah, Burmeister, Margit, Chapman, Sinéad, DelaBastide, Melissa, Juréus, Anders, Kang, Hyun Min, Kwok, Pui-Yan, Li, Jun Z., Levy, Shawn E., Monson, Eric T., Moran, Jennifer, Sobell, Janet, Watson, Stanley, Willour, Virginia, Zöllner, Sebastian, Adolfsson, Rolf, Blackwood, Douglas, Boehnke, Michael, Breen, Gerome, Corvin, Aiden, Craddock, Nick, DiFlorio, Arianna, Hultman, Christina M., Landen, Mikael, Lewis, Cathryn, McCarroll, Steven A., Richard McCombie, W., McGuffin, Peter, McIntosh, Andrew, McQuillin, Andrew, Morris, Derek, Myers, Richard M., O’Donovan, Michael, Ophoff, Roel, Boks, Marco, Kahn, Rene, Ouwehand, Willem, Owen, Michael, Pato, Carlos, Pato, Michele, Posthuma, Danielle, Potash, James B., Reif, Andreas, Sklar, Pamela, Smoller, Jordan, Sullivan, Patrick F., Vincent, John, Walters, James, Neale, Benjamin, Purcell, Shaun, Risch, Neil, Schaefer, Catherine, Stahl, Eli A., Zandi, Peter P., and Scott, Laura J.

Published
2021
Full Text
View/download PDF

24. The genetics of severe depression

Author

Franklin, Clio E., Achtyes, Eric, Altinay, Murat, Bailey, Kala, Bhati, Mahendra T., Carr, Brent R., Conroy, Susan K., Husain, Mustafa M., Khurshid, Khurshid A., Lencz, Todd, McDonald, William M., Mickey, Brian J., Murrough, James, Nestor, Sean, Nickl-Jockschat, Thomas, Nikayin, Sina, Reeves, Kevin, Reti, Irving M., Selek, Salih, Sanacora, Gerard, Trapp, Nicholas T., Viswanath, Biju, Wright, Jesse H., Sullivan, Patrick, Zandi, Peter P., and Potash, James B.

Abstract

Genome-wide association studies (GWASs) of major depressive disorder (MDD) have recently achieved extremely large sample sizes and yielded substantial numbers of genome-wide significant loci. Because of the approach to ascertainment and assessment in many of these studies, some of these loci appear to be associated with dysphoria rather than with MDD, potentially decreasing the clinical relevance of the findings. An alternative approach to MDD GWAS is to focus on the most severe forms of MDD, with the hope that this will enrich for loci of larger effect, rendering their identification plausible, and providing potentially more clinically actionable findings. Here we review the genetics of severe depression by using clinical markers of severity including: age of onset, recurrence, degree of impairment, and treatment with ECT. There is evidence for increased family-based and Single Nucleotide Polymorphism (SNP)-based estimates of heritability in recurrent and early-onset illness as well as severe functional impariment. GWAS have been performed looking at severe forms of MDD and a few genome-wide loci have been identified. Several whole exome sequencing studies have also been performed, identifying associated rare variants. Although these findings have not yet been rigorously replicated, the elevated heritability seen in severe MDD phenotypes suggests the value of pursuing additional genome-wide interrogation of samples from this population. The challenge now is generating a cohort of adequate size with consistent phenotyping that will allow for careful and robust classifications and distinctions to be made. We are currently pursuing such a strategy in our 50-site worldwide Gen-ECT-ics consortium.

Published
2024
Full Text
View/download PDF

25. Low-intensity ultrasound restores long-term potentiation and memory in senescent mice through pleiotropic mechanisms including NMDAR signaling

Author

Blackmore, Daniel G., Turpin, Fabrice, Palliyaguru, Tishila, Evans, Harrison T., Chicoteau, Antony, Lee, Wendy, Pelekanos, Matthew, Nguyen, Nghia, Song, Jae, Sullivan, Robert K. P., Sah, Pankaj, Bartlett, Perry F., and Götz, Jürgen

Abstract

Advanced physiological aging is associated with impaired cognitive performance and the inability to induce long-term potentiation (LTP), an electrophysiological correlate of memory. Here, we demonstrate in the physiologically aged, senescent mouse brain that scanning ultrasound combined with microbubbles (SUS+MB), by transiently opening the blood–brain barrier, fully restores LTP induction in the dentate gyrus of the hippocampus. Intriguingly, SUS treatment without microbubbles (SUSonly), i.e., without the uptake of blood-borne factors, proved even more effective, not only restoring LTP, but also ameliorating the spatial learning deficits of the aged mice. This functional improvement is accompanied by an altered milieu of the aged hippocampus, including a lower density of perineuronal nets, increased neurogenesis, and synaptic signaling, which collectively results in improved spatial learning. We therefore conclude that therapeutic ultrasound is a non-invasive, pleiotropic modality that may enhance cognition in elderly humans.

Published
2024
Full Text
View/download PDF

26. Correction: Common-variant associations with fragile X syndrome

Author

Crowley, James J., Szatkiewicz, Jin, Kähler, Anna K., Giusti-Rodriguez, Paola, Ancalade, NaEshia, Booker, Jessica K., Carr, Jennifer L., Giamberardino, Stephanie N., Crawford, Greg E., Losh, Molly, Stockmeier, Craig A., Taylor, Annette K., Piven, Joseph, and Sullivan, Patrick F.

Published
2020
Full Text
View/download PDF

27. Gene expression in major depressive disorder

Author

Jansen, R, Penninx, B W J H, Madar, V, Xia, K, Milaneschi, Y, Hottenga, J J, Hammerschlag, A R, Beekman, A, van der Wee, N, Smit, J H, Brooks, A I, Tischfield, J, Posthuma, D, Schoevers, R, van Grootheest, G, Willemsen, G, de Geus, E J, Boomsma, D I, Wright, F A, Zou, F, Sun, W, and Sullivan, P F

Published
2016
Full Text
View/download PDF

28. Low-intensity ultrasound restores long-term potentiation and memory in senescent mice through pleiotropic mechanisms including NMDAR signaling

Author

Wendy Lee, Nghia Q. Nguyen, Jürgen Götz, Fabrice R. Turpin, Tishila Palliyaguru, Pankaj Sah, Daniel G. Blackmore, Perry F. Bartlett, Harrison Tudor Evans, Matthew Pelekanos, Antony Chicoteau, Jae Song, and Robert K. P. Sullivan

Subjects
0301 basic medicine, Neurogenesis, Long-Term Potentiation, Hippocampus, Receptors, N-Methyl-D-Aspartate, Biochemistry, Article, Mice, 03 medical and health sciences, Cellular and Molecular Neuroscience, Cognition, 0302 clinical medicine, LTP induction, Animals, Medicine, Molecular Biology, business.industry, Dentate gyrus, Perineuronal net, Long-term potentiation, Psychiatry and Mental health, 030104 developmental biology, NMDA receptor, Synaptic signaling, business, Neuroscience, 030217 neurology & neurosurgery
Abstract

Advanced physiological aging is associated with impaired cognitive performance and the inability to induce long-term potentiation (LTP), an electrophysiological correlate of memory. Here, we demonstrate in the physiologically aged, senescent mouse brain that scanning ultrasound combined with microbubbles (SUS+MB), by transiently opening the blood–brain barrier, fully restores LTP induction in the dentate gyrus of the hippocampus. Intriguingly, SUS treatment without microbubbles (SUSonly), i.e., without the uptake of blood-borne factors, proved even more effective, not only restoring LTP, but also ameliorating the spatial learning deficits of the aged mice. This functional improvement is accompanied by an altered milieu of the aged hippocampus, including a lower density of perineuronal nets, increased neurogenesis, and synaptic signaling, which collectively results in improved spatial learning. We therefore conclude that therapeutic ultrasound is a non-invasive, pleiotropic modality that may enhance cognition in elderly humans.

Published
2021
Full Text
View/download PDF

29. A genome-wide association study of anorexia nervosa

Author

Boraska, V, Franklin, C S, Floyd, J A B, Thornton, L M, Huckins, L M, Southam, L, Rayner, N W, Tachmazidou, I, Klump, K L, Treasure, J, Lewis, C M, Schmidt, U, Tozzi, F, Kiezebrink, K, Hebebrand, J, Gorwood, P, Adan, R A H, Kas, M J H, Favaro, A, Santonastaso, P, Fernández-Aranda, F, Gratacos, M, Rybakowski, F, Dmitrzak-Weglarz, M, Kaprio, J, Keski-Rahkonen, A, Raevuori, A, Van Furth, E F, Slof-Op 't Landt, M C T, Hudson, J I, Reichborn-Kjennerud, T, Knudsen, G P S, Monteleone, P, Kaplan, A S, Karwautz, A, Hakonarson, H, Berrettini, W H, Guo, Y, Li, D, Schork, N J, Komaki, G, Ando, T, Inoko, H, Esko, T, Fischer, K, Männik, K, Metspalu, A, Baker, J H, Cone, R D, Dackor, J, DeSocio, J E, Hilliard, C E, O'Toole, J K, Pantel, J, Szatkiewicz, J P, Taico, C, Zerwas, S, Trace, S E, Davis, O S P, Helder, S, Bühren, K, Burghardt, R, de Zwaan, M, Egberts, K, Ehrlich, S, Herpertz-Dahlmann, B, Herzog, W, Imgart, H, Scherag, A, Scherag, S, Zipfel, S, Boni, C, Ramoz, N, Versini, A, Brandys, M K, Danner, U N, de Kovel, C, Hendriks, J, Koeleman, B P C, Ophoff, R A, Strengman, E, van Elburg, A A, Bruson, A, Clementi, M, Degortes, D, Forzan, M, Tenconi, E, Docampo, E, Escaramís, G, Jiménez-Murcia, S, Lissowska, J, Rajewski, A, Szeszenia-Dabrowska, N, Slopien, A, Hauser, J, Karhunen, L, Meulenbelt, I, Slagboom, P E, Tortorella, A, Maj, M, Dedoussis, G, Dikeos, D, Gonidakis, F, Tziouvas, K, Tsitsika, A, Papezova, H, Slachtova, L, Martaskova, D, Kennedy, J L, Levitan, R D, Yilmaz, Z, Huemer, J, Koubek, D, Merl, E, Wagner, G, Lichtenstein, P, Breen, G, Cohen-Woods, S, Farmer, A, McGuffin, P, Cichon, S, Giegling, I, Herms, S, Rujescu, D, Schreiber, S, Wichmann, H-E, Dina, C, Sladek, R, Gambaro, G, Soranzo, N, Julia, A, Marsal, S, Rabionet, R, Gaborieau, V, Dick, D M, Palotie, A, Ripatti, S, Widén, E, Andreassen, O A, Espeseth, T, Lundervold, A, Reinvang, I, Steen, V M, Le Hellard, S, Mattingsdal, M, Ntalla, I, Bencko, V, Foretova, L, Janout, V, Navratilova, M, Gallinger, S, Pinto, D, Scherer, S W, Aschauer, H, Carlberg, L, Schosser, A, Alfredsson, L, Ding, B, Klareskog, L, Padyukov, L, Courtet, P, Guillaume, S, Jaussent, I, Finan, C, Kalsi, G, Roberts, M, Logan, D W, Peltonen, L, Ritchie, G R S, Barrett, J C, Estivill, X, Hinney, A, Sullivan, P F, Collier, D A, Zeggini, E, and Bulik, C M

Published
2014
Full Text
View/download PDF

31. Copy number variation in schizophrenia in Sweden

Author

Szatkiewicz, J P, O'Dushlaine, C, Chen, G, Chambert, K, Moran, J L, Neale, B M, Fromer, M, Ruderfer, D, Akterin, S, Bergen, S E, Kähler, A, Magnusson, P K E, Kim, Y, Crowley, J J, Rees, E, Kirov, G, O'Donovan, M C, Owen, M J, Walters, J, Scolnick, E, Sklar, P, Purcell, S, Hultman, C M, McCarroll, S A, and Sullivan, P F

Published
2014
Full Text
View/download PDF

32. Allelic differences between Europeans and Chinese for CREB1 SNPs and their implications in gene expression regulation, hippocampal structure and function, and bipolar disorder susceptibility

Author

Li, M, Luo, X-j, Rietschel, M, Lewis, C M, Mattheisen, M, Müller-Myhsok, B, Jamain, S, Leboyer, M, Landén, M, Thompson, P M, Cichon, S, Nöthen, M M, Schulze, T G, Sullivan, P F, Bergen, S E, Donohoe, G, Morris, D W, Hargreaves, A, Gill, M, Corvin, A, Hultman, C, Toga, A W, Shi, L, Lin, Q, Shi, H, Gan, L, Meyer-Lindenberg, A, Czamara, D, Henry, C, Etain, B, Bis, J C, Ikram, M A, Fornage, M, Debette, S, Launer, L J, Seshadri, S, Erk, S, Walter, H, Heinz, A, Bellivier, F, Stein, J L, Medland, S E, Arias Vasquez, A, Hibar, D P, Franke, B, Martin, N G, Wright, M J, and Su, B

Published
2014
Full Text
View/download PDF

33. Correction: Investigation of common, low-frequency and rare genome-wide variation in anorexia nervosa

Author

Huckins, L M, Hatzikotoulas, K, Southam, L, Thornton, L M, Steinberg, J, Aguilera-McKay, F, Treasure, J, Schmidt, U, Gunasinghe, C, Romero, A, Curtis, C, Rhodes, D, Moens, J, Kalsi, G, Dempster, D, Leung, R, Keohane, A, Burghardt, R, Ehrlich, S, Hebebrand, J, Hinney, A, Ludolph, A, Walton, E, Deloukas, P, Hofman, A, Palotie, A, Palta, P, van Rooij, F J A, Stirrups, K, Adan, R, Boni, C, Cone, R, Dedoussis, G, van Furth, E, Gonidakis, F, Gorwood, P, Hudson, J, Kaprio, J, Kas, M, Keski-Rahonen, A, Kiezebrink, K, Knudsen, G-P, Maj, M, Monteleone, A M, Monteleone, P, Raevuori, A H, Reichborn-Kjennerud, T, Tozzi, F, Tsitsika, A, van Elburg, A, Collier, D A, Sullivan, P F, Breen, G, Bulik, C M, and Zeggini, E

Published
2018
Full Text
View/download PDF

36. Meta-analysis of genome-wide association studies for personality

Author

de Moor, M H M, Costa, P T, Terracciano, A, Krueger, R F, de Geus, E J C, Toshiko, T, Penninx, B W J H, Esko, T, Madden, P A F, Derringer, J, Amin, N, Willemsen, G, Hottenga, J-J, Distel, M A, Uda, M, Sanna, S, Spinhoven, P, Hartman, C A, Sullivan, P, Realo, A, Allik, J, Heath, A C, Pergadia, M L, Agrawal, A, Lin, P, Grucza, R, Nutile, T, Ciullo, M, Rujescu, D, Giegling, I, Konte, B, Widen, E, Cousminer, D L, Eriksson, J G, Palotie, A, Peltonen, L, Luciano, M, Tenesa, A, Davies, G, Lopez, L M, Hansell, N K, Medland, S E, Ferrucci, L, Schlessinger, D, Montgomery, G W, Wright, M J, Aulchenko, Y S, Janssens, A C J W, Oostra, B A, Metspalu, A, Abecasis, G R, Deary, I J, Räikkönen, K, Bierut, L J, Martin, N G, van Duijn, C M, and Boomsma, D I

Published
2012
Full Text
View/download PDF

37. GWA study data mining and independent replication identify cardiomyopathy-associated 5 (CMYA5) as a risk gene for schizophrenia

Author

Chen, X, Lee, G, Maher, B S, Fanous, A H, Chen, J, Zhao, Z, Guo, A, van den Oord, E, Sullivan, P F, Shi, J, Levinson, D F, Gejman, P V, Sanders, A, Duan, J, Owen, M J, Craddock, N J, O'Donovan, M C, Blackman, J, Lewis, D, Kirov, G K, Qin, W, Schwab, S, Wildenauer, D, Chowdari, K, Nimgaonkar, V, Straub, R E, Weinberger, D R, O'Neill, F A, Walsh, D, Bronstein, M, Darvasi, A, Lencz, T, Malhotra, A K, Rujescu, D, Giegling, I, Werge, T, Hansen, T, Ingason, A, Nöethen, M M, Rietschel, M, Cichon, S, Djurovic, S, Andreassen, O A, Cantor, R M, Ophoff, R, Corvin, A, Morris, D W, Gill, M, Pato, C N, Pato, M T, Macedo, A, Gurling, H M D, McQuillin, A, Pimm, J, Hultman, C, Lichtenstein, P, Sklar, P, Purcell, S M, Scolnick, E, St Clair, D, Blackwood, D H R, and Kendler, K S

Published
2011
Full Text
View/download PDF

39. Fine mapping of ZNF804A and genome-wide significant evidence for its involvement in schizophrenia and bipolar disorder

Author

Williams, H J, Norton, N, Dwyer, S, Moskvina, V, Nikolov, I, Carroll, L, Georgieva, L, Williams, N M, Morris, D W, Quinn, E M, Giegling, I, Ikeda, M, Wood, J, Lencz, T, Hultman, C, Lichtenstein, P, Thiselton, D, Maher, B S, Malhotra, A K, Riley, B, Kendler, K S, Gill, M, Sullivan, P, Sklar, P, Purcell, S, Nimgaonkar, V L, Kirov, G, Holmans, P, Corvin, A, Rujescu, D, Craddock, N, Owen, M J, and O'Donovan, M C

Published
2011
Full Text
View/download PDF

45. Variants in Apaf-1 segregating with major depression promote apoptosome function

Author

Harlan, J, Chen, Y, Gubbins, E, Mueller, R, Roch, J-M, Walter, K, Lake, M, Olsen, T, Metzger, P, Dorwin, S, Ladror, U, Egan, D A, Severin, J, Johnson, R W, Holzman, T F, Voelp, K, Davenport, C, Beck, A, Potter, J, Gopalakrishnan, M, Hahn, A, Spear, B B, Halbert, D N, Sullivan, J P, Abkevich, V, Neff, C D, Skolnick, M H, Shattuck, D, and Katz, D A

Published
2006
Full Text
View/download PDF

49. Meta-analysis of genome-wide association data of bipolar disorder and major depressive disorder

Author

Liu, Y, Blackwood, D H, Caesar, S, de Geus, E J C, Farmer, A, Ferreira, M A R, Ferrier, I N, Fraser, C, Gordon-Smith, K, Green, E K, Grozeva, D, Gurling, H M, Hamshere, M L, Heutink, P, Holmans, P A, Hoogendijk, W J, Hottenga, J J, Jones, L, Jones, I R, Kirov, G, Lin, D, McGuffin, P, Moskvina, V, Nolen, W A, Perlis, R H, Posthuma, D, Scolnick, E M, Smit, A B, Smit, J H, Smoller, J W, St Clair, D, van Dyck, R, Verhage, M, Willemsen, G, Young, A H, Zandbelt, T, Boomsma, D I, Craddock, N, O'Donovan, M C, Owen, M J, Penninx, B W J H, Purcell, S, Sklar, P, and Sullivan, P F

Published
2011
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results