Biology subjects

Rodrigue, K.

Publications and source records attributed to Rodrigue, K..

3 recordsLinked to original sources

bioRxiv2026

Brain Structure-Function Association as a Compensatory Factor in Cognitive Aging

Functional activity in response to increasing task difficulty (BOLD-modulation) in regions of the default mode network (DMN/task-negative) and multiple demand network (MDN/task-positive) shows age-related decline, which is associated with reduced cognitive performance. While BOLD-modulation in the DMN begins to decline in middle-age, white matter structural connectivity declines earlier in MDN regions. We conjecture that to maintain executive function (EF) performance with aging, altered BOLD-modulation in DMN during task engagement serves as a compensatory reaction to structural decline in MDN. To test this possibility, functionally-guided tractography was applied in 160 healthy adults aged 20-94 to locate white matter connecting MDN and/or DMN regions that were active during a distance judgement paradigm. Specifically, analyses examined the effects of 1) age on white matter tracts (fractional anisotropy; FA); 2) structure-function association between FA and BOLD-modulation; and 3) age, positive/negative BOLD-modulation, and quadratic FA on EF. Age-related decline was found in one MDN tract (U-shaped tract) and a significant structure-function association was found in inferior fronto-occipital fasciculus (IFOF). Additionally, an interaction effect between quadratic frontal-insular (U-shaped) tract FA, age, and positive/negative BOLD-modulation was found for inhibition performance, supporting the hypothesis of compensatory functional activity effects on executive function for older adults with altered white matter microstructure.

neuroscience↗

bioRxiv2023

Differential effects of aging on regional corpus callosum microstructure and the modifying influence of pulse pressure

The corpus callosum is composed of several subregions, distinct in cellular and functional organization. This organization scheme may render these subregions differentially vulnerable to the aging process. Callosal integrity may be further compromised by vascular risk factors, which negatively influence white matter health. Here, we test for heterochronicity of aging, hypothesizing an anterior-to-posterior gradient of vulnerability to aging that may be altered by effects of vascular health. In 174 healthy adults across the adult lifespan (mean age=53.56 {+/-} 18.90, range=20-94 years old, 58.62% women), measures of pulse pressure and diffusion-weighted imaging were conducted. A deterministic tractography approach was utilized to extract fractional anisotropy (FA), radial diffusivity (RD) and axial diffusivity (AD) from each of five callosal subregions, serving as estimates of microstructural health. General linear models tested effects of age, hypertension, and pulse pressure on these metrics. We observed no significant effect of hypertensive diagnosis on callosal microstructure. We found a significant main effect of age and an age x pulse pressure interaction whereby older age and elevated pulse pressure were associated with poorer FA, AD, and RD. Age effects revealed non-linear components and occurred along an anterior-posterior gradient of severity in the callosum. This gradient disappeared when pulse pressure was considered. These results indicate that age-related deterioration across the callosum is regionally variable, and that pulse pressure, a proxy of arterial stiffness, alters this aging pattern. Significance StatementAging is associated with microstructural changes in the corpus callosum, the largest white matter tract in the brain. Additionally, vascular factors, such as hypertension and pulse pressure, affect corpus callosum microstructure. However, it is unclear whether these factors uniformly impact the corpus callosum throughout aging. The current study aimed to characterize patterns of aging and assess the role of hypertension and pulse pressure across different subregions of the corpus callosum. We found an age-related gradient on corpus callosum microstructure, with the most pronounced impact on anterior regions. However, this gradient was not found when pulse pressure was considered. These findings suggest that subregions are differentially sensitive to age-related decline, and pulse pressure modifies and exacerbates these declines.

neuroscience↗

bioRxiv2019

Joint contributions of cortical morphometry and white matter microstructure in healthy brain aging: A partial least squares correlation analysis

Cortical atrophy and degraded axonal health have been shown to coincide during normal aging; however, few studies have examined these measures together. To lend insight into both the regional specificity and the relative timecourse of structural degradation of these tissue compartments across the lifespan, we analyzed grey matter (GM) morphometry (cortical thickness, surface area, volume) and estimates of white matter (WM) microstructure (fractional anisotropy, mean diffusivity) using traditional univariate and more robust multivariate techniques to examine age associations in 186 healthy adults aged 20-94 years old. Univariate analysis of each tissue type revealed that negative age associations were largest in frontal grey and white matter tissue and weaker in temporal, cingulate, and occipital regions, representative of not only an anterior-to-posterior gradient, but also a medial-to-lateral gradient. Multivariate partial least squares correlation (PLSC) found the greatest covariance between GM and WM was driven by the relationship between WM metrics in the anterior corpus callosum and projections of the genu, anterior cingulum, and fornix; and with GM thickness in parietal and frontal regions. Surface area was far less susceptible to age effects and displayed less covariance with WM metrics, while regional volume covariance patterns largely mirrored those of cortical thickness. Results support a retrogenesis-like model of aging, revealing a coupled relationship between frontal and parietal GM and the underlying WM, which evidence the most protracted development and the most vulnerability during healthy aging.

neuroscience↗