Publication Title: 
Journal of Psychiatric Research

DNA methylation is an important epigenetic mechanism for gene regulation and it is well established there is association between aging and DNA methylation. Alzheimer's disease (AD) is the most common neurodegenerative disease, characterized by amyloid plaque deposition and formation of neurofibrillary tangles. In this study, we examined the correlation between DNA methylation and gene expression of seven genes including CTSB, CTSD, DDT, TSC1, NRD1, UQCRC1 and NDUFA6 and its effect on the risk of AD in a Chinese population.

Ma, Suk Ling
Tang, Nelson Leung Sang
Lam, Linda Chiu Wa
Publication Title: 
Biological Research

Schizophrenia is a severe psychiatric disorder that results in a significant disability for the patient. The disorder is characterized by impairment of the adaptive orchestration of actions, a cognitive function that is mainly dependent on the prefrontal cortex. This behavioral deficit, together with cellular and neurophysiological alterations in the prefrontal cortex, as well as reduced density of GABAergic cells and aberrant oscillatory activity, all indicate structural and functional deficits of the prefrontal cortex in schizophrenia.

NegrÛn-Oyarzo, Ignacio
Lara-V·squez, Ariel
Palacios-GarcÌa, Ismael
Fuentealba, Pablo
Aboitiz, Francisco
Publication Title: 
Nature Neuroscience

By analyzing the whole-exome sequences of 4,264 schizophrenia cases, 9,343 controls and 1,077 trios, we identified a genome-wide significant association between rare loss-of-function (LoF) variants in SETD1A and risk for schizophrenia (P = 3.3 ◊ 10(-9)). We found only two heterozygous LoF variants in 45,376 exomes from individuals without a neuropsychiatric diagnosis, indicating that SETD1A is substantially depleted of LoF variants in the general population. Seven of the ten individuals with schizophrenia carrying SETD1A LoF variants also had learning difficulties.

Singh, Tarjinder
Kurki, Mitja I.
Curtis, David
Purcell, Shaun M.
Crooks, Lucy
McRae, Jeremy
Suvisaari, Jaana
Chheda, Himanshu
Blackwood, Douglas
Breen, Gerome
Pietil‰inen, Olli
Gerety, Sebastian S.
Ayub, Muhammad
Blyth, Moira
Cole, Trevor
Collier, David
Coomber, Eve L.
Craddock, Nick
Daly, Mark J.
Danesh, John
DiForti, Marta
Foster, Alison
Freimer, Nelson B.
Geschwind, Daniel
Johnstone, Mandy
Joss, Shelagh
Kirov, Georg
Kˆrkkˆ, Jarmo
Kuismin, Outi
Holmans, Peter
Hultman, Christina M.
Iyegbe, Conrad
Lˆnnqvist, Jouko
M‰nnikkˆ, Minna
McCarroll, Steve A.
McGuffin, Peter
McIntosh, Andrew M.
McQuillin, Andrew
Moilanen, Jukka S.
Moore, Carmel
Murray, Robin M.
Newbury-Ecob, Ruth
Ouwehand, Willem
Paunio, Tiina
Prigmore, Elena
Rees, Elliott
Roberts, David
Sambrook, Jennifer
Sklar, Pamela
St Clair, David
Veijola, Juha
Walters, James T. R.
Williams, Hywel
Swedish Schizophrenia Study
DDD Study
UK10 K Consortium
Sullivan, Patrick F.
Hurles, Matthew E.
O'Donovan, Michael C.
Palotie, Aarno
Owen, Michael J.
Barrett, Jeffrey C.
Publication Title: 
Nature Communications

DNA methylation likely plays a role in the regulation of human stress reactivity. Here we show that in a genome-wide analysis of blood DNA methylation in 85 healthy individuals, a locus in the Kit ligand gene (KITLG; cg27512205) showed the strongest association with cortisol stress reactivity (P=5.8 ◊ 10(-6)). Replication was obtained in two independent samples using either blood (N=45, P=0.001) or buccal cells (N=255, P=0.004). KITLG methylation strongly mediates the relationship between childhood trauma and cortisol stress reactivity in the discovery sample (32% mediation).

Houtepen, Lotte C.
Vinkers, Christiaan H.
Carrillo-Roa, Tania
Hiemstra, Marieke
van Lier, Pol A.
Meeus, Wim
Branje, Susan
Heim, Christine M.
Nemeroff, Charles B.
Mill, Jonathan
Schalkwyk, Leonard C.
Creyghton, Menno P.
Kahn, RenÈ S.
JoÎls, Marian
Binder, Elisabeth B.
Boks, Marco P. M.
Publication Title: 
Depression and Anxiety

BACKGROUND: DNA methylation of the SKA2 gene has recently been implicated as a biomarker of suicide risk and posttraumatic stress disorder (PTSD). To examine the specificity and reliability of these findings, we examined associations between SKA2 DNA methylation, broad dimensions of psychiatric symptoms, and suicide phenotypes in adults with high levels of trauma exposure. METHODS: A total of 466 White, non-Hispanic veterans and their intimate partners (65% male) underwent clinical assessment and had blood drawn for genotyping and methylation analysis.

Sadeh, Naomi
Wolf, Erika J.
Logue, Mark W.
Hayes, Jasmeet P.
Stone, Annjanette
Griffin, L. Michelle
Schichman, Steven A.
Miller, Mark W.
Publication Title: 
Proceedings of the National Academy of Sciences of the United States of America

Recent studies have identified impairments in neural induction and in striatal and cortical neurogenesis in Huntington's disease (HD) knock-in mouse models and associated embryonic stem cell lines. However, the potential role of these developmental alterations for HD pathogenesis and progression is currently unknown. To address this issue, we used BACHD:CAG-Cre(ERT2) mice, which carry mutant huntingtin (mHtt) modified to harbor a floxed exon 1 containing the pathogenic polyglutamine expansion (Q97).

Molero, Aldrin E.
Arteaga-Bracho, Eduardo E.
Chen, Christopher H.
Gulinello, Maria
Winchester, Michael L.
Pichamoorthy, Nandini
Gokhan, Solen
Khodakhah, Kamran
Mehler, Mark F.
Publication Title: 
Clinical Epigenetics

Bipolar disorder (BD) and schizophrenia (SZ) are known to share common genetic and psychosocial risk factors. A recent epigenome-wide association study performed on blood samples from SZ patients found significant hypomethylation of FAM63B in exon 9. Here, we used iPLEX-based methylation analysis to investigate two CpG sites in FAM63B in blood samples from 459 BD cases and 268 controls. Both sites were significantly hypomethylated in BD cases (lowest p value?=?3.94 ◊ 10(-8)).

Starnawska, Anna
Demontis, Ditte
McQuillin, Andrew
O'Brien, Niamh L.
Staunstrup, Nicklas H.
Mors, Ole
Nielsen, Anders L.
B¯rglum, Anders D.
Nyegaard, Mette
Publication Title: 
Psychiatria Danubina

Posttraumatic Stress Disorder (PTSD) is a major health problem in South Eastern Europe (SEE). Available treatment options are not efficient enough and the course is often chronic. Little is known about molecular mediators and moderators of pathogenesis and therapy. Genetic and epigenetic variation may be one central molecular mechanism.

Kulenovic, Alma Dzubur
Agani, Ferid
Avdibegovic, Esmina
Jakovljevic, Miro
Babic, Dragan
Kucukalic, Abdulah
Kucukalic, Sabina
Dzananovic, Emina Sabic
Mehmedbasic, Alma Bravo
Uka, Aferdita Goci
Haxhibeqiri, Shpend
Haxhibeqiri, Valdete
Hoxha, Blerina
Sinanovic, Osman
Kravic, Nermina
Muminovic, Mirnesa
Aukst-Margetic, Branka
Jaksic, Nenad
Franc, Ana Cima
Rudan, Dusko
Pavlovic, Marko
Babic, Romana
Bojic, Elma Feric
Marjanovic, Damir
Bozina, Nada
Ziegler, Christiane
Wolf, Christiane
Warrings, Bodo
Domschke, Katharina
Deckert, J¸rgen
Publication Title: 
Clinical Epigenetics

BACKGROUND: In utero and early-life experienced environmental exposures are suggested to play an important role in many multifactorial diseases potentially mediated through lasting effects on the epigenome. As the epigenome in addition remains modifiable throughout life, identifying specific disease-relevant biomarkers may prove challenging. This has led to an increased interest in epigenome-wide association studies using dried blood spots (DBS) routinely collected in perinatal screening programs.

Staunstrup, Nicklas H.
Starnawska, Anna
Nyegaard, Mette
Christiansen, Lene
Nielsen, Anders L.
B¯rglum, Anders
Mors, Ole
Publication Title: 

The development of the brain depends on an individual's nature (genes) and nurture (environments). This interaction between genetic predispositions and environmental events during brain development drives the maturation of functional brain circuits such as sensory, motor, emotional, and complex cognitive pathways. Adverse environmental conditions such as early life stress can interfere with the functional development of emotional and cognitive brain systems and thereby increase the risk of developing psychiatric disorders later in life.

Matas, Emmanuel
Bock, Jˆrg
Braun, Katharina


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