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Recent research suggests that individuals with multiple sclerosis (MS) and cognitive impairment exhibit more effortful and less efficient transitions in brain network activity. Previous studies further highlight the increased vulnerability of specific regions, particularly the thalamus, to disease-related damage. This study investigates whether MS affects the controllability of specific brain regions in driving network activity transitions across the brain and examines the relationship between these changes and cognitive impairment in patients. Resting-state functional MRI and neuropsychological data were collected from 102 MS and 27 healthy controls. Functional network controllability analysis was performed to quantify how specific regions influence transitions between brain activity patterns or states. Disease alterations in controllability were assessed in the main dataset and then replicated in an independent dataset of 95 MS and 45 healthy controls. Controllability metrics were then used to distinguish MS from healthy controls and predict cognitive status. MS-specific controllability changes were observed in the subcortical network, particularly the thalamus, which were further confirmed in the replication dataset. Cognitively impaired patients showed significantly greater difficulty in the thalamus steering brain transitions towards difficult-to-reach states, which are typically associated with high-energy-cost cognitive functions. Thalamic network controllability proved more effective than thalamic volume in distinguishing MS from healthy controls (AUC = 88.3%), and in predicting cognitive status in MS (AUC = 80.7%). This study builds on previous research highlighting early thalamic damage in MS, aiming to demonstrate how this damage disrupts activity transitions across the cerebrum and may predict cognitive deficits. Our findings suggest that the thalamus in MS becomes less capable of facilitating broader brain activity transitions essential for high-energy-cost cognitive functions, implying a potential pathological mechanism that links thalamic functional changes to cognitive impairment in MS.
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http://dx.doi.org/10.1002/hbm.70284 | DOI Listing |
Psychopharmacology (Berl)
September 2025
División de Neurociencias, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Ciudad Universitaria, Mexico City, 04510, Mexico.
Rationale: One of the earliest changes associated with Alzheimer's disease (AD) is the loss of catecholaminergic terminals in the cortex and hippocampus originating from the Locus Coeruleus (LC). This decline leads to reduced catecholaminergic neurotransmitters in the hippocampus, affecting synaptic plasticity and spatial memory. However, it is unclear whether restoring catecholaminergic transmission in the terminals from the LC may alleviate the spatial memory deficits associated with AD.
View Article and Find Full Text PDFNaunyn Schmiedebergs Arch Pharmacol
September 2025
Pharmacology and Toxicology Department, Faculty of Pharmacy and Biotechnology, German University in Cairo, Gamal Abdel Nasser, 11835, New Cairo, Egypt.
Licochalcone A (LCA), a natural flavonoid with potent anti-inflammatory properties, has shown promise as a neuroprotective agent. However, its ability to cross the blood-brain barrier (BBB) and exert central effects remains underexplored. In this study, we demonstrate for the first time that LCA enhances cognitive function in a lipopolysaccharide (LPS)-induced neuroinflammatory mouse model and effectively penetrates the BBB.
View Article and Find Full Text PDFNeurol Res
September 2025
Electrophysiology Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran.
Objectives: This study aimed to investigate the effects of repeated exposure to sevoflurane as an anesthetic agent during various developmental stages, namely neonatal, preadolescent, and adult, on behavioral, synaptic, and neuronal plasticity in male and female Wistar rats.
Methods: Rats were exposed to sevoflurane during three developmental stages: neonatal (PN7), pre-adolescence (PN28), and adulthood (PN90). Behavioral performance was evaluated with the Morris Water Maze.
Radiology
September 2025
Department of Radiology and Radiological Sciences, Johns Hopkins University, Baltimore, Md.
Background Elevated brain iron is a potential marker for neurodegeneration, but its role in predicting onset of mild cognitive impairment (MCI) and prospective cognitive trajectories remains unclear. Purpose To investigate how brain iron and amyloid-β (Aβ) levels, measured using quantitative susceptibility mapping (QSM) MRI and PET, help predict MCI onset and cognitive decline. Materials and Methods In this prospective study conducted between January 2015 and November 2022, cognitively unimpaired older adults underwent baseline QSM MRI.
View Article and Find Full Text PDFRadiology
September 2025
Boston University, VA Boston Health Care System, Boston Medical Center, One Boston Medical Center Place, Boston, MA 02118.