Epigenetic epidemiology in psychiatry: A translational neuroscience perspective

Abstract

Introductiondifferential epigenetic profiles) for epigenetic involvement in the most prevalent and severe psychiatric illnesses. We will end the article by discussing current research challenges in epigenetic epidemiology and neuroscience, and we propose that more studies combining epidemiological and neuroscience approaches in studying epigenetics are needed to improve our understanding of the role of the epigenetic machinery in the etiologies of psychiatric disorders. Besides robust changes in reprogramming of genomic methylation patterns in germline cells as well as in pre-implantation embryos [78]. In autism, a 10-year increase in paternal age (independent of maternal age) was associated with a 22% increased risk for autism (independent of paternal age) while a 10-year increase in maternal age has been associated with a 38% increased risk for developing the disorder [78,79], which is in line with other findings reporting associations between parental ages and autism [80][81][82]. A recent metaanalysis on the association between paternal age and schizophrenia reported that both advanced paternal age (>/=30) and younger paternal age (<25) may increase the risk of schizophrenia, with further analyses indicating that younger paternal age may be associated with particularly an increased risk in male but not female offspring [83]. Given these effects of paternal (and maternal age) on risk of several psychiatric disorders, one could speculate that Epigenetic mechanisms Epigenetics and sex differences in psychiatric disorders Environmental epigenetic in psychiatric disordersA wealth of epidemiologic evidence indicates that environmental exposures influence susceptibility to disease in later life [19,49].

Monoaminergic neuropathology in Alzheimer’s disease

“…Animal data suggest that these neurochemical and behavioral changes in adults may have their origins in perinatal exposure, e.g. to 5-HT precursor 5-hydroxytriptophan, 5-HTP, or MAO inhibitors (Blažević and Hranilović, 2013), as well as other pre- and postnatal factors, most likely via epigenetic mechanisms (Pishva et al, 2012). Such changes have also been described as a part of the clinical picture in very early stages of AD (Cummings, 1992; Mychack et al, 2001; Michelsen, 2008).…”

Epigenetic Genes and Emotional Reactivity to Daily Life Events: A Multi-Step Gene-Environment Interaction Study

“…A growing body of evidence from human and animal studies suggests that the ability to regulate emotions is influenced by genetic liability, environmental exposures over the life course, as well as personality traits and coping styles. While the biological basis of emotion regulation and inter-individual variability in the response to stress remains incompletely understood, a flux of recent investigations has shown that epigenetic regulation of gene expression can mediate experience-dependent plasticity (structural and functional changes in the brain in response to environmental exposures and experiences) [3] and may thus play a crucial role in regulating the impact of environmental exposures on psychological and biological functioning of the individual [4] . DNA methylation, that is, the chemical addition of methyl groups to nucleotides, is a key epigenetic mechanism influencing gene expression.…”