Back to the future: omnipresence of fetal influence on the human brain through the lifespan

Abstract

Human fetal development has been associated with brain health at later stages. It is unknown whether and how consistently growth in utero, as indexed by birth weight (BW), relates to lifespan brain characteristics and changes, and to what extent these influences are of a genetic and/or environmental nature. We hypothesized that associations of BW and structural brain characteristics persist through the lifespan, with topographically consistent effects across samples of varying age and origin, that BW is not protective against atrophy in aging, and that effects are partly environmental. The associations of BW and cortical area, thickness, volume and their change were investigated vertex-wise in developmental (ABCD), older adult and aging (UKB) and lifespan (LCBC) longitudinal samples. In total, 5794 persons (4-82 years, w/ 386 monozygotic twins), were followed for up to 8.3 years, yielding 12,088 brain MRIs. Positive associations between BW and cortical surface area and volume were remarkably stable through the lifespan, within and across samples of different origin, with spatial correlations in the range r = .51- .79. In contrast, there was modest and no consistent effect of BW on brain changes. Effects of BW discordance in the monozygotic twin subsample indicated the effects were partly environmental. In conclusion, the influence of prenatal growth on cortical topography is stable through the lifespan, and is reliably seen in development, adulthood, and aging. These findings support early life influence on the brain through the lifespan according to a threshold model of brain reserve, rather than a maintenance model.

Reliability of structural brain change in cognitively healthy adult samples

“…Cross-sectional measurement error. Measurement error σε was estimated as the average error across six different test-retest cohorts consisting of cognitively healthy adult participants, namely, the S2C (Walhovd et al, 2024), the preventAD (Orban et al, 2015), OASIS (Marcus et al, 2007), and GSP (Holmes et al, 2015) reliability subsets, and the HNU1 (Chen et al, 2015) and Maclaren (Maclaren et al, 2014) mean to the between-subject average for test-retest and to the within-subject average for densely scanned designs) were discarded. Measurement error (𝜎 𝑒 ) was estimated for a given subject (i) as the absolute difference between each measure estimated from both sessions divided by the mean of the two for test-retest designs (eq.…”

Genetic and brain similarity independently predict childhood anthropometrics and socioeconomic markers

“…It remains uncertain if estimates of morphometricity would be equally reduced. As a growing body of evidence demonstrates associations between perinatal and early-life factors and later brain development (Alnaes et al 2020;Walhovd et al 2023), we also included weight at birth.…”

Current perspectives on perinatal mental health and neurobehavioral development: focus on regulation, coregulation and self-regulation

“…Data from the World Mental Health Surveys [1 ▪ ] indicate that the lifetime prevalence of any mental disorder is 28.6% for females and 29.8 for males, with age of onset often during childhood and adolescence [1 ▪ ]. A range of evidence – including brain imaging studies [2], genetic studies [3] and studies combining brain imaging and early gene expression [4] - indicate that mental disorders are associated with altered brain developmental processes even earlier, beginning in pregnancy. The period encompassing pregnancy and the first two years after birth -the perinatal period- has also been termed ‘the first 1000 days’ or ‘the first 1001 critical days’.…”