1.
Whole-Brain Dynamics in Aging: Disruptions in Functional Connectivity and the Role of the Rich Club.
Escrichs, A, Biarnes, C, Garre-Olmo, J, Fernández-Real, JM, Ramos, R, Pamplona, R, Brugada, R, Serena, J, Ramió-Torrentà, L, Coll-De-Tuero, G, et al
Cerebral cortex (New York, N.Y. : 1991). 2021;(5):2466-2481
Abstract
Normal aging causes disruptions in the brain that can lead to cognitive decline. Resting-state functional magnetic resonance imaging studies have found significant age-related alterations in functional connectivity across various networks. Nevertheless, most of the studies have focused mainly on static functional connectivity. Studying the dynamics of resting-state brain activity across the whole-brain functional network can provide a better characterization of age-related changes. Here, we employed two data-driven whole-brain approaches based on the phase synchronization of blood-oxygen-level-dependent signals to analyze resting-state fMRI data from 620 subjects divided into two groups (middle-age group (n = 310); age range, 50-64 years versus older group (n = 310); age range, 65-91 years). Applying the intrinsic-ignition framework to assess the effect of spontaneous local activation events on local-global integration, we found that the older group showed higher intrinsic ignition across the whole-brain functional network, but lower metastability. Using Leading Eigenvector Dynamics Analysis, we found that the older group showed reduced ability to access a metastable substate that closely overlaps with the so-called rich club. These findings suggest that functional whole-brain dynamics are altered in aging, probably due to a deficiency in a metastable substate that is key for efficient global communication in the brain.
2.
Redox lipidomics to better understand brain aging and function.
Pamplona, R, Borras, C, Jové, M, Pradas, I, Ferrer, I, Viña, J
Free radical biology & medicine. 2019;:310-321
Abstract
Human prefrontal cortex (PFC) is a recently evolutionary emerged brain region involved in cognitive functions. Human cognitive abilities decline during aging. Yet the molecular mechanisms that sustain the preservation or deterioration of neurons and PFC functions are unknown. In this review, we focus on the role of lipids in human PFC aging. As the evolution of brain lipid concentrations is particularly accelerated in the human PFC, conferring a specific lipid profile, a brief approach to the lipidome of PFC was consider along with the relationship between lipids and lipoxidative damage, and the role of lipids in human PFC aging. In addition, the specific targets of lipoxidative damage in human PFC, the affected biological processes, and their potential role in the cognitive decline associated with aging are discussed. Finally, interventions designed to modify this process are considered. We propose that the dysfunction of key biological processes due to selective protein lipoxidation damage may have a role the cognitive decline of PFC during aging.