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Background
Early life adversity and psychiatric disorders are associated with earlier declines in neurocognitive abilities during adulthood. These declines may be preceded by changes in biological aging, specifically epigenetic age acceleration, providing an opportunity to uncover genome-wide biomarkers that identify individuals most likely to bene...
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Context 1
... genotypes were used to derive the polygenic score for educational attainment using summary statistics as per standard protocol ( Lee et al., 2018). See Supplemental Table 2 for further details on genotyping used in the FGDS and BeCOME cohorts. Childhood Maltreatment Status. ...Context 2
... diagrams of results from the FGDS and BeCOME cohorts are in Figs Table 2 for the general pattern of results across clocks and between cohorts. ...Context 3
... all six analyses, we controlled for the most prominent risk factors for cognitive impairment and variables that explain extraneous variation in epigenetic age acceleration estimates. We found evidence that epigenetic age acceleration was associated with neurocognitive functioning, although these associations depended upon which clock was investigated in each cohort (see Table 2 for the side-by-side comparison of the findings). Based on the strengths of this study and corresponding results, there are several important directions for future research with patients treated for child maltreatment or psychiatric disorders. ...Citations
... Alémdisso, observa-se que indivíduos expostos a ambientes cotidianos atribulados e instáveis durante suas infâncias tendem a apresentar mudanças em mecanismos fisiológicos e neuropatológicos e, assim, alteram suas idades epigenéticas. Com isso, tem-se um cenário de divergência entre a idade biológica e a idade epigenética destes indivíduos, que, devido a esse contexto, tendem a apresentar deficits em suas expressões cognitivas durante a vida adulta(FELT et al., 2023).Tambémé válido ressaltar que estudos constataram que, a partir das análises de dados coletados por Enlow et al, Strathearn et al e Richards e Wadsworth, indivíduos expostos a experiencias traumáticas entre 0 e 24 meses de vida, apresentaram deficits no desempenho cognitivo entre as idades de 24 a 96 meses, que maus-tratos nos primeiros anos de vida apresentam reflexos no desempenho intelectual individual e que crianças que passaram por eventos traumáticos como a morte de um dos genitores ou o divórcio dos pais tendem a apresentar uma menor performance intelectual entre os 8 e 15 anos de idade (OH et al., 2018). As modificações nas histonas, proteínas que ajudam a estruturar o DNA, também desempenham um papel crucial na regulação dos genes. ...
Este artigo tem como seus objetos de estudo os fatores epigenéticos envolvidos na expressão da cognição humana e busca oferecer uma compilação do conhecimento científico acerca dos aspectos epigenéticos associados à manifestação cognitiva. Nesse ínterim, foi realizada uma revisão de literatura com a coleta de 21 artigos produzidos entre 2018 e 2024, que apresentam como constatações principais os fatos de que, a partir de modificações epigenéticas, provocadas por fatores ambientais, nos padrões de metilação, de acetilação, de histonas e de expressão dos miRNAs, observam-se impactos na expressão intelectual individual que podem se relacionar direta ou indiretamente a estes mecanismos epigenéticos ou então a patologias neurológicas como o Alzheimer. Logo, com a compreensão destes fatores cognitivos, tem-se o cerne para pesquisas de terapias que visem a manutenção cognitiva com o envelhecimento.
... A growing body of evidence suggests that such indicators of more rapid epigenetic aging may also be associated with developmental measures in children. Youth with greater EAA are more likely to have experienced stress/adverse childhood experiences 22 with future cognitive impairment 23 and depression and anxiety 24 . Our report adds to the growing body of work that examines EAA with respect to childhood markers of growth and maturation. ...
Using data from a longitudinal cohort of children, we examined whether epigenetic age acceleration (EAA) was associated with pubertal growth and whether these associations were mediated by adiposity. We examined associations between EAA at approximately 10 years of age with pubertal growth metrics, including age at peak height velocity (PHV), PHV, and sex steroid levels and whether these associations were mediated by measures of adiposity including body mass index (BMI) and MRI-assessed visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT). Children (n = 135) with accelerated EAA had higher PHV (β 0.018, p = 0.0008) although the effect size was small. The association between EAA and age at PHV was not significant (β − 0.0022, p = 0.067). Although EAA was associated with higher BMI (β 0.16, p = 0.0041), VAT (β 0.50, p = 0.037), and SAT (β 3.47, p = 0.0076), BMI and VAT did not mediate associations between EAA and PHV, while SAT explained 8.4% of the association. Boys with higher EAA had lower total testosterone (β − 12.03, p = 0.0014), but associations between EAA and other sex steroids were not significant, and EAA was not associated with sex steroid levels in girls. We conclude that EAA did not have strong associations with either age at onset of puberty or pubertal growth speed, although associations with growth speed were statistically significant. Studies with larger sample sizes are needed to confirm this pattern of associations.
This article studies the epigenetic factors involved in the expression of human cognition and seeks to provide a compilation of scientific knowledge about the epigenetic aspects associated with cognitive manifestation. In the meantime, a literature review was carried out with the collection of 21 articles produced between 2018 and 2024, which present as main findings the facts that, from epigenetic modifications, caused by environmental factors, in the patterns of methylation, acetylation, histones and expression of miRNAs, impacts are observed on individual intellectual expression that can be directly or indirectly related to these epigenetic mechanisms or to neurological pathologies such as Alzheimer's. Therefore, with the understanding of these cognitive factors, we have the core for research into therapies that aim at cognitive maintenance with aging.
Childhood exposure to interparental intimate partner violence (i-IPV) is a pervasive form of child maltreatment, posing major public health concerns and elevating risks for enduring adverse clinical and developmental consequences. However, assessing the full spectrum of clinical effects is challenging, potentially leading to inconsistent identification of children in need of early intervention. This systematic review aimed to identify hypothalamic-pituitary-adrenocortical axis dysfunction following i-IPV exposure, elucidating the underlying biopsychobehavioural mechanisms and predicting adverse outcomes. We searched Embase, MEDLINE, and PsycINFO for peer-reviewed studies from infancy through adolescence, screened reference lists and conducted forward searches. Analysis of 23 publications (N = 1848) revealed associations between i-IPV and altered adrenocortical function from early childhood, influenced by FKBP5 haplotype, parental caregiving and offspring emotional insecurity. Results showed that the adrenocortical stress response may predict internalising and externalising problems, childhood asthma, impaired executive function and poor academic performance. Nonetheless, inconsistencies in findings between studies suggest methodological heterogeneity and potential bias. Identifying biomarkers such as cortisol can enhance prediction and mechanism-based intervention efforts but long-term studies with a common theoretical and methodological framework are needed for comprehensive understanding. Integrating biological, emotional, and behavioural assessments could potentiate trauma services and research, ultimately improving outcomes for affected children.
Background
Childhood abuse is an underappreciated source of stress, associated with adverse mental and physical health consequences. Childhood abuse has been directly associated with risky behavior thereby increasing the likelihood of alcohol misuse and risk of HIV infection, conditions associated with brain structural and functional deficits. Here, we examined the neural and behavioral correlates of childhood trauma history in alcohol use disorder (AUD), HIV infection (HIV), and their comorbidity (AUD+HIV).
Methods
Occurrence of childhood trauma was evaluated by retrospective interview. Cortical (frontal, temporal, parietal, and occipital), subcortical (hippocampus, amygdala), and regional frontal volumes were derived from structural MRI, adjusted for intracranial volume and age. Test scores of executive functioning, attention/working memory, verbal/visual learning, verbal/visual memory, and motor speed functional domains were standardized on age and education of a laboratory control group.
Results
History of childhood abuse was associated with smaller frontal lobe volumes regardless of diagnosis. For frontal subregional volumes, history of childhood abuse was selectively associated with smaller orbitofrontal and supplementary motor volumes. In participants with a child abuse history, poorer verbal/visual memory performance was associated with smaller orbitofrontal and frontal middle volumes, whereas in those without childhood abuse, poorer verbal/visual memory performance was associated with smaller orbitofrontal, frontal superior, and supplemental motor volumes.
Conclusions
Taken together, these results comport with and extend the findings that childhood abuse is associated with brain and behavioral sequelae in AUD, HIV, and AUD+HIV comorbidity. Further, these findings suggest that sequelae of abuse in childhood may be best conceptualized as a spectrum disorder as significant deficits may be present in those who may not meet criteria for a formal trauma-related diagnosis yet may be suffering enduring stress effects on brain structural and functional health.
