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Network analytical tools are increasingly being applied to brain imaging maps of resting metabolic activity (PET) or blood oxygenation-dependent signals (functional MRI) to characterize the abnormal neural circuitry that underlies brain diseases. This approach is particularly valuable for the study of neurodegenerative disorders, which are characterized by stereotyped spread of pathology along discrete neural pathways. Identification and validation of disease-specific brain networks facilitate the quantitative assessment of pathway changes over time and during the course of treatment. Network abnormalities can often be identified before symptom onset and can be used to track disease progression even in the preclinical period. Likewise, network activity can be modulated by treatment and might therefore be used as a marker of efficacy in clinical trials. Finally, early differential diagnosis can be achieved by simultaneously measuring the activity levels of multiple disease networks in an individual patient's scans. Although these techniques were originally developed for PET, over the past several years analogous methods have been introduced for functional MRI, a more accessible non-invasive imaging modality. This advance is expected to broaden the application of network tools to large and diverse patient populations.
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http://dx.doi.org/10.1038/s41582-022-00753-3 | DOI Listing |
Phys Rev Lett
August 2025
Northeastern University, Department of Physics, Center for Theoretical Biological Physics, Boston, Massachusetts 02115, USA.
Sparse connectivity is a hallmark of the brain and a desired property of artificial neural networks. It promotes energy efficiency, simplifies training, and enhances the robustness of network function. Thus, a detailed understanding of how to achieve sparsity without jeopardizing network performance is beneficial for neuroscience, deep learning, and neuromorphic computing applications.
View Article and Find Full Text PDFSci Adv
September 2025
Movement Disorder and Neuromodulation Unit, Department of Neurology, Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
Subthalamic deep brain stimulation (STN-DBS) provides unprecedented spatiotemporal precision for the treatment of Parkinson's disease (PD), allowing for direct real-time state-specific adjustments. Inspired by findings from optogenetic stimulation in mice, we hypothesized that STN-DBS can mimic dopaminergic reinforcement of ongoing movement kinematics during stimulation. To investigate this hypothesis, we delivered DBS bursts during particularly fast and slow movements in 24 patients with PD.
View Article and Find Full Text PDFPLoS Comput Biol
September 2025
Faculty of Science, Cognitive and Systems Neuroscience Group, Swammerdam Institute for Life Sciences, University of Amsterdam, Amsterdam, the Netherlands.
Predictive coding (PC) proposes that our brains work as an inference machine, generating an internal model of the world and minimizing predictions errors (i.e., differences between external sensory evidence and internal prediction signals).
View Article and Find Full Text PDFBrain
September 2025
Sorbonne University, Inserm U1127, CNRS UMR7225, UM75, Paris Brain Institute, Movement Investigation and Therapeutics Team, 75013 Paris, France.
Adolescence is frequently called the second brain maturation period. In Tourette disorder (TD), the clinical trajectory of tics and associated psychiatric co-morbidities vary significantly across individuals during the transition from adolescents to adulthood. In this study, we aimed to identify patterns of resting-state functional connectivity that differentiate adolescents with TD from their neurotypical peers, and to monitor symptom-specific functional changes over time.
View Article and Find Full Text PDFBrain
September 2025
Departamento de Fisiología, Facultad de Medicina, Universidad de Granada, 18016 Granada, Spain.
Primary coenzyme Q (CoQ) deficiency is a mitochondrial disorder with variable clinical presentation and limited response to standard CoQ10 supplementation. Recent studies suggest that 4-hydroxybenzoic acid (4-HBA), a biosynthetic precursor of CoQ, may serve as a substrate enhancement treatment in cases caused by pathogenic variants in COQ2, a gene encoding a key enzyme in CoQ biosynthesis. However, it remains unclear whether 4-HBA is required throughout life to maintain health, whether it offers advantages over CoQ10 treatment, and whether these findings are translatable to humans.
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