Early life adversity linked to accelerated neurobiological aging, raising vulnerability to depression and Alzheimer's

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Early life adversity linked to accelerated neurobiological aging, raising vulnerability to depression and Alzheimer's
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Early life adversity linked to accelerated neurobiological aging, raising vulnerability to depression and Alzheimer's Alzheimers Disease Children DepressiveDisorder Depression MajorDepressiveDisorder SciReports LivUni cardiffuni

By Dr. Priyom Bose, Ph.D.Mar 30 2023Reviewed by Benedette Cuffari, M.Sc. Neural development is affected by early life adversity , which includes poverty and mistreatment or neglect by caregivers. One of the key mechanisms through which ELA inhibits optimal brain functioning is systemic low-grade inflammation. Moreover, ELA accelerates cellular senescence through DNA methylation of stress genes, which enhances the long-term risk for psychiatric and neurodegenerative disorders.

In addition, both MDD and ADD are strongly connected to prior stress exposure, along with a modest genetic relation. Synaptic transmission impairment in the prefrontal cortex is another factor for cognitive control deficits that cause AD and MDD. The majority of studies on brain correlates of AD and/or MDD risk factors have focused on individuals raised by their birth families. These studies fail to distinguish between genetic and non-genetic contributions of the manifested phenotypes.

To this end, the authors compared the profiles of children in their late childhood with profiles of adoptees and non-adoptees. Adoptees are those who were not raised by their biological parents, while non-adoptees are children who were raised by their biological parents. Children recruited in this study participated in the Adolescent Brain and Cognitive Development study.

Two AD GRSs were considered, in which the first apolipoprotein E AD GRS included only the APOE region, whereas the second excluded the APOE region. These two AD GRSs were computed to investigate neurocognitive impairments trajectories and variance in susceptibility to environmental factors. Cortical thickness was considered to determine the structural neurodevelopmental timing due to its well-defined maturational trajectory, which is regulated by genes and is susceptible to ELA. Among non-adoptees, a significant GRS-brain association was found, thus indicating that this group had a greater vulnerability to AD and/or MDD. In addition, this group exhibited reduced vigor in neural activity on inhibitory control tasks.

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