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Aging-related cognitive decline can be accelerated by a combination of genetic factors, cardiovascular and cerebrovascular dysfunction, and amyloid-β burden. Whereas cerebral blood flow (CBF) has been studied as a potential early biomarker of cognitive decline, its normal variability in healthy elderly is less known. In this study, we investigated the contribution of genetic, vascular, and amyloid-β components of CBF in a cognitively unimpaired (CU) population of monozygotic older twins. We included 134 participants who underwent arterial spin labeling (ASL) MRI and [18F]flutemetamol amyloid-PET imaging at baseline and after a four-year follow-up. General estimating equations were used to investigate the associations of amyloid burden and white matter hyperintensities with CBF. We showed that, in CU individuals, CBF: 1) has a genetic component, as within-pair similarities in CBF values were moderate and significant (ICC>0.40); 2) is negatively associated with cerebrovascular damage; and 3) is positively associated with the interaction between cardiovascular risk scores and early amyloid-β burden, which may reflect a vascular compensatory response of CBF to early amyloid-β accumulation. These findings encourage future studies to account for multiple interactions with CBF in disease trajectory analyses.

BACKGROUND Amide proton transfer (APT) imaging is a chemical exchange saturation transfer (CEST) technique offering potential clinical applications in patients with brain tumors. PURPOSE To investigate whether cerebral APT-CEST is sufficiently reproducible in healthy tissue and glioma for clinical use at 3T. STUDY TYPE Prospective, longitudinal SUBJECTS Twenty-one healthy volunteers (M:F = 10:11; age 39±11 years) and six glioma patients (M:F = 3:3; age 50±17 years: four glioblastomas, one oligodendroglioma, one suspected low-grade glioma). FIELD STRENGTH/SEQUENCE 3T, SPACE-CEST ASSESSMENT APT-CEST measurement reproducibility was assessed within-session (glioma patients, healthy volunteers), and between-sessions and between-days (healthy volunteers). The standard deviation of the within-subject difference (SDdiff) was calculated in tumor regions of interest (ROI), and eight ROIs at relevant locations including a whole-brain ROI. STATISTICAL TESTS Brown-Forsythe tests and variance component analyses (VCA) were used to assess the reproducibility of ROIs for the three reproducibility time intervals. Intraclass correlation coefficient (ICC) was used to assess agreement between the ROIs for the three reproducibility time intervals. RESULTS APT-CEST magnetization transfer ratio asymmetry (MTRasym) was 0.89±0.96% on average in healthy brain tissue and 1.59±0.67% in tumor tissue. Intratumoral mean MTRasym was significantly higher than MTRasym in healthy-appearing tissue in patients (0.5±0.46%; P< 0.001). The APTCEST difference between GBMs and contralateral tissue was 1.11%. The average within-session, between-sessions, and between-days SDdiff of healthy control brains was 0.2%. The within-session SDdiff of whole-brain was 0.2% in both healthy volunteers and patients, and 0.21% in the segmented tumor. The orbitofrontal gyri were the ROI with the highest within-session SDdiff (0.61%). Within-session reproducibility of ROIs did not differ significantly from between-sessions or between-day reproducibility (0.76>P>0.22) and VCA showed that within-session variance was the most important factor (60%), but differed from between-days reproducibility in putamen and the central brain (P

International audience; A combined experimental and numerical investigation of the roughness of intergranular cracks in two-dimensional disordered solids is presented. We focus on brittle materials for which the characteristic length scale of damage is much smaller than the grain size. Surprisingly, brittle cracks do not follow a persistent path with a roughness exponent ζ ≈ 0.6-0.7 as reported for a large range of materials. Instead, we show that they exhibit mono-affine scaling properties characterized by a roughness exponent ζ = 0.5 ± 0.05, which we explain theoretically from linear elastic fracture mechanics. Our findings support the description of the roughening process in two-dimensional brittle disordered solids by a random walk. Furthermore, they shed light on the failure mechanism at the origin of the persistent behavior with ζ ≈ 0.6-0.7 observed for fractures in other materials, suggesting a unified scenario for the geometry of cracks paths in two-dimensional disordered solids.