Redundancy protects processing speed in healthy individuals with accelerated brain aging.

Recent advancements in computational learning techniques have enabled the estimation of brain age (BA) from neuroimaging data. The difference between chronological age (CA) and BA, known as the BA gap, can potentially serve as a biomarker of brain health. Studies, however, have documented low correlations between BA gap and cognition in healthy aging.

Lasting differential gene expression of circulating CD8 T cells in chronic HCV infection with cirrhosis identifies a role for Hedgehog signaling in cellular hyperfunction.

Background: The impact of chronic hepatic infection on antigen non-specific immune cells in circulation remains poorly understood. We reported lasting global hyperfunction of peripheral CD8 T cells in HCV-infected individuals with cirrhosis. Whether gene expression patterns in bulk CD8 T cells are associated with the severity of liver fibrosis in HCV infection is not known.

Age-related differences in network controllability are mitigated by redundancy in large-scale brain networks.

The aging brain undergoes major changes in its topology. The mechanisms by which the brain mitigates age-associated changes in topology to maintain robust control of brain networks are unknown. Here we use diffusion MRI data from cognitively intact participants (n = 480, ages 40-90) to study age-associated differences in the average controllability of structural brain networks, topological features that could mitigate these differences, and the overall effect on cognitive function.

Progeria-based vascular model identifies networks associated with cardiovascular aging and disease.

Hutchinson-Gilford Progeria syndrome (HGPS) is a lethal premature aging disorder caused by a de novo heterozygous mutation that leads to the accumulation of a splicing isoform of Lamin A termed progerin. Progerin expression deregulates the organization of the nuclear lamina and the epigenetic landscape. Progerin has also been observed to accumulate at low levels during normal aging in cardiovascular cells of adults that do not carry genetic mutations linked with HGPS.