scholarly journals Author Correction: Dynamic causal modelling of immune heterogeneity

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Thomas Parr ◽  
Anjali Bhat ◽  
Peter Zeidman ◽  
Aimee Goel ◽  
Alexander J. Billig ◽  
...  
NeuroImage ◽  
2010 ◽  
Vol 52 (4) ◽  
pp. 1456-1464 ◽  
Author(s):  
Sébastien Reyt ◽  
Chloé Picq ◽  
Valérie Sinniger ◽  
Didier Clarençon ◽  
Bruno Bonaz ◽  
...  

NeuroImage ◽  
2009 ◽  
Vol 47 ◽  
pp. S168 ◽  
Author(s):  
M Woolrich ◽  
T Behrens ◽  
S Jbabdi

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Elia Benhamou ◽  
Charles R. Marshall ◽  
Lucy L. Russell ◽  
Chris J. D. Hardy ◽  
Rebecca L. Bond ◽  
...  

Abstract The selective destruction of large-scale brain networks by pathogenic protein spread is a ubiquitous theme in neurodegenerative disease. Characterising the circuit architecture of these diseases could illuminate both their pathophysiology and the computational architecture of the cognitive processes they target. However, this is challenging using standard neuroimaging techniques. Here we addressed this issue using a novel technique—spectral dynamic causal modelling—that estimates the effective connectivity between brain regions from resting-state fMRI data. We studied patients with semantic dementia—the paradigmatic disorder of the brain system mediating world knowledge—relative to healthy older individuals. We assessed how the effective connectivity of the semantic appraisal network targeted by this disease was modulated by pathogenic protein deposition and by two key phenotypic factors, semantic impairment and behavioural disinhibition. The presence of pathogenic protein in SD weakened the normal inhibitory self-coupling of network hubs in both antero-mesial temporal lobes, with development of an abnormal excitatory fronto-temporal projection in the left cerebral hemisphere. Semantic impairment and social disinhibition were linked to a similar but more extensive profile of abnormally attenuated inhibitory self-coupling within temporal lobe regions and excitatory projections between temporal and inferior frontal regions. Our findings demonstrate that population-level dynamic causal modelling can disclose a core pathophysiological feature of proteinopathic network architecture—attenuation of inhibitory connectivity—and the key elements of distributed neuronal processing that underwrite semantic memory.


Author(s):  
Amirhossein Jafarian ◽  
Peter Zeidman ◽  
Vladimir Litvak ◽  
Karl Friston

Identifying a coupled dynamical system out of many plausible candidates, each of which could serve as the underlying generator of some observed measurements, is a profoundly ill-posed problem that commonly arises when modelling real-world phenomena. In this review, we detail a set of statistical procedures for inferring the structure of nonlinear coupled dynamical systems (structure learning), which has proved useful in neuroscience research. A key focus here is the comparison of competing models of network architectures—and implicit coupling functions—in terms of their Bayesian model evidence. These methods are collectively referred to as dynamic causal modelling. We focus on a relatively new approach that is proving remarkably useful, namely Bayesian model reduction, which enables rapid evaluation and comparison of models that differ in their network architecture. We illustrate the usefulness of these techniques through modelling neurovascular coupling (cellular pathways linking neuronal and vascular systems), whose function is an active focus of research in neurobiology and the imaging of coupled neuronal systems. This article is part of the theme issue ‘Coupling functions: dynamical interaction mechanisms in the physical, biological and social sciences'.


NeuroImage ◽  
2015 ◽  
Vol 107 ◽  
pp. 117-126 ◽  
Author(s):  
Margarita Papadopoulou ◽  
Marco Leite ◽  
Pieter van Mierlo ◽  
Kristl Vonck ◽  
Louis Lemieux ◽  
...  

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