NeuroImage
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The human connectome refers to a map of the brain's structural connections, rendered as a connection matrix or network. This article attempts to trace some of the historical origins of the connectome, in the process clarifying its definition and scope, as well as its putative role in illuminating brain function. Current efforts to map the connectome face a number of significant challenges, including the issue of capturing network connectivity across multiple spatial scales, accounting for individual variability and structural plasticity, as well as clarifying the role of the connectome in shaping brain dynamics. Throughout, the article argues that these challenges require the development of new approaches for the statistical analysis and computational modeling of brain network data, and greater collaboration across disciplinary boundaries, especially with researchers in complex systems and network science.
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It was 20 years ago that Crick and Jones lamented the fact that human neuroanatomy was backward. They would be astonished to read the contents of this issue. At that time they had not foreseen what could be achieved by the combination of diffusion imaging and the study of resting state covariance. This paper assesses what can and cannot be done with the methods that we now have.
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Low-frequency temporal fluctuations of physiological signals (<0.1 Hz), such as the respiration and cardiac pulse rate, occur naturally during rest and have been shown to be correlated with blood-oxygenation-level-dependent (BOLD) signal fluctuation. Such physiological signal modulations have been considered as sources of noise and their effects on BOLD signal are commonly removed in functional magnetic resonance imaging (fMRI) studies. However, possible neural correlates of the physiological fluctuations have not been considered nor examined in detail. ⋯ Similar spatial patterns were observed between the correlation maps of BOLD with alpha EEG power and respiration, with negative correlations coinciding in the visual cortex, superior/middle temporal gyrus, inferior frontal gyrus, and inferior parietal lobule and positive correlations in the thalamus and caudate. Regressing out the physiological variations in the BOLD signal resulted in reduced correlation between BOLD and alpha EEG power. These results suggest a mutual link of neuronal origin between alpha EEG power, respiration, and BOLD signals.
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From a neuroimaging point of view, deep brain stimulation (DBS) in psychiatric disorders represents a unique source of information to probe results gained in functional, structural and molecular neuroimaging studies in vivo. However, the implementation has, up to now, been restricted by the heterogeneity of the data reported in DBS studies. The aim of the present study was therefore to provide a comprehensive and standardized database of currently used DBS targets in selected psychiatric disorders (obsessive-compulsive disorder (OCD), treatment-resistant depression (TRD), Gilles de la Tourette syndrome (GTS)) to enable topological comparisons between neuroimaging results and stimulation areas. ⋯ Vice versa, the structural, functional and molecular data may provide a rationale to define new DBS targets and adjust/fine-tune currently used targets in DBS based on this overview in stereotactic coordinates. Furthermore, the availability of DBS data in stereotactic space may facilitate the investigation and interpretation of treatment effects and side effect of DBS by comparing these to neuroimaging results. The present study thus improves comparability between functional, structural and molecular data in standard stereotactic space gained in neuroimaging studies with surgical targets for DBS, which is among other possible implications of crucial importance for the definition of new targets for effective DBS.
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A previous clinical trial studied the effect of long-term treatment with levodopa (LD) or the dopamine agonist pramipexole (PPX) on disease progression in Parkinson disease using SPECT with the dopamine transporter (DAT)-radioligand [(123)I]β-CIT as surrogate marker. [(123)I]β-CIT binding declined to significantly lower levels in patients receiving LD compared to PPX. However, the interpretation of this difference as LD-induced neurotoxicity, PPX-induced neuroprotection/-regeneration, or only drug-induced regulatory changes of DAT-availability remained controversial. To address this question experimentally, we induced a subtotal lesion of the substantia nigra in mice by bilateral injection of the neurotoxin 6-hydroxydopamine. ⋯ In 6-hydroxydopamine-lesioned mice, however, neither LD nor PPX significantly influenced the stably reduced FP-CIT SPECT signal (LD: -66%; PPX: -66%; controls -66%), TH-immunoreactivity (LD: -70%; PPX: -72%; controls: -77%) and DAT-immunoreactivity (LD: -70%; PPX: -75%; controls: -75%) in the striatum or the number of TH-positive cells in the substantia nigra (LD: -88%; PPX: -88%; controls: -86%), compared to lesioned mice without dopaminergic treatment. In conclusion, chronic dopaminergic stimulation with LD or PPX induced similar adaptive presynaptic changes in healthy mice, but no discernible changes in severely lesioned mice. These findings allow to more reliably interpret the results from clinical trials using neuroimaging of DAT as surrogate parameter.