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There have been successful applications of deep learning to functional magnetic resonance imaging (fMRI), where fMRI data were mostly considered to be structured grids, and spatial features from Euclidean neighbors were usually extracted by the convolutional neural networks (CNNs) in the computer vision field. Recently, CNN has been extended to graph data and demonstrated superior performance. Here, we define graphs based on functional connectivity and present a connectivity-based graph convolutional network (cGCN) architecture for fMRI analysis. Such an approach allows us to extract spatial features from connectomic neighborhoods rather than from Euclidean ones, consistent with the functional organization of the brain. To evaluate the performance of cGCN, we applied it to two scenarios with resting-state fMRI data. One is individual identification of healthy participants and the other is classification of autistic patients from normal controls. Our results indicate that cGCN can effectively capture functional connectivity features in fMRI analysis for relevant applications.

Patients with Parkinson’s disease undergo a loss of melanized neurons in substantia nigra pars compacta and locus coeruleus. Very few studies have assessed substantia nigra pars compacta and locus coeruleus pathology in Parkinson’s disease simultaneously with magnetic resonance imaging (MRI). Neuromelanin-sensitive MRI measures of substantia nigra pars compacta and locus coeruleus volume based on explicit magnetization transfer contrast have been shown to have high scan-rescan reproducibility in controls, but no study has replicated detection of Parkinson’s disease-associated volume loss in substantia nigra pars compacta and locus coeruleus in multiple cohorts with the same methodology. Two separate cohorts of Parkinson’s disease patients and controls were recruited from the Emory Movement Disorders Clinic and scanned on two different MRI scanners. In cohort 1, imaging data from 19 controls and 22 Parkinson’s disease patients were acquired with a Siemens Trio 3 Tesla scanner using a 2D gradient echo sequence with magnetization transfer preparation pulse. Cohort 2 consisted of 33 controls and 39 Parkinson’s disease patients who were scanned on a Siemens Prisma 3 Tesla scanner with a similar imaging protocol. Locus coeruleus and substantia nigra pars compacta volumes were segmented in both cohorts. Substantia nigra pars compacta volume (Cohort 1: p = 0.0148; Cohort 2: p = 0.0011) and locus coeruleus volume (Cohort 1: p = 0.0412; Cohort 2: p = 0.0056) were significantly reduced in the Parkinson’s disease group as compared to controls in both cohorts. This imaging approach robustly detects Parkinson’s disease effects on these structures, indicating that it is a promising marker for neurodegenerative neuromelanin loss.

The diagnosis of Parkinson’s disease (PD) occurs after pathogenesis is advanced and many substantia nigra (SN) dopamine neurons have already died. Now that therapies to block this neuronal loss are under development, it is imperative that the disease be diagnosed at earlier stages and that the response to therapies is monitored. Recent studies suggest this can be accomplished by magnetic resonance imaging (MRI) detection of neuromelanin (NM), the characteristic pigment of SN dopaminergic, and locus coeruleus (LC) noradrenergic neurons. NM is an autophagic product synthesized via oxidation of catecholamines and subsequent reactions, and in the SN and LC it increases linearly during normal aging. In PD, however, the pigment is lost when SN and LC neurons die. As shown nearly 25 years ago by Zecca and colleagues, NM’s avid binding of iron provides a paramagnetic source to enable electron and nuclear magnetic resonance detection, and thus a means for safe and noninvasive measure in living human brain. Recent technical improvements now provide a means for MRI to differentiate between PD patients and age-matched healthy controls, and should be able to identify changes in SN NM with age in individuals. We discuss how MRI detects NM and how this approach might be improved. We suggest that MRI of NM can be used to confirm PD diagnosis and monitor disease progression. We recommend that for subjects at risk for PD, and perhaps generally for older people, that MRI sequences performed at regular intervals can provide a pre-clinical means to detect presymptomatic PD.

Neurocognitive aging researchers are increasingly focused on the locus coeruleus, a neuromodulatory brainstem structure that degrades with age. With this rapid growth, the field will benefit from consensus regarding which magnetic resonance imaging (MRI) metrics of locus coeruleus structure are most sensitive to age and cognition. To address this need, the current study acquired magnetization transfer- and diffusion-weighted MRI images in younger and older adults who also completed a free recall memory task. Results revealed significantly larger differences between younger and older adults for maximum than average magnetization transfer-weighted contrast (MTC), axial than mean or radial single-tensor diffusivity (DTI), and free than restricted multi-compartment diffusion (NODDI) metrics in the locus coeruleus; with maximum MTC being the best predictor of age group. Age effects for all imaging modalities interacted with sex, with larger age group differences in males than females for MTC and NODDI metrics. Age group differences also varied across locus coeruleus subdivision for DTI and NODDI metrics, and across locus coeruleus hemispheres for MTC. Within older adults, however, there were no significant effects of age on MTC or DTI metrics, only an interaction between age and sex for free diffusion. Finally, independent of age and sex, higher restricted diffusion in the locus coeruleus was significantly related to better (lower) recall variability, but not mean recall. Whereas MTC has been widely used in the literature, our comparison between the average and maximum MTC metrics, inclusion of DTI and NODDI metrics, and breakdowns by locus coeruleus subdivision and hemisphere make important and novel contributions to our understanding of the aging of locus coeruleus structure.

Cytokine effects on behavior may be related to alterations in glutamate metabolism. We therefore measured glutamate concentrations in brain regions shown to be affected by inflammatory stimuli including the cytokine interferon (IFN)-alpha. IFN-alpha is known to alter neural activity in the dorsal anterior cingulate cortex (dACC) and basal ganglia in association with symptoms of depression and increases in peripheral cytokines including the tumor necrosis factor (TNF) and its soluble receptor. Single-voxel magnetic resonance spectroscopy (MRS) was employed to measure glutamate concentrations normalized to creatine (Glu/Cr) in dACC and basal ganglia of 31 patients with hepatitis C before and after ∼ 1 month of either no treatment (n = 14) or treatment with IFN-alpha (n = 17). Depressive symptoms were measured at each visit using the Inventory of Depressive Symptoms-Clinician Rating (IDS-C) and the Multidimensional Fatigue Inventory. IFN-alpha was associated with a significant increase in Glu/Cr in dACC and left basal ganglia. Increases in dACC Glu/Cr were positively correlated with scores on the IDS-C in the group as a whole, but not in either group alone. Glu/Cr increases in left basal ganglia were correlated with decreased motivation in the group as a whole and in IFN-alpha-treated subjects alone. No Glu/Cr changes were found in the right basal ganglia, and no significant correlations were found between Glu/Cr and the inflammatory markers. IFN-alpha-induced increases in glutamate in dACC and basal ganglia are consistent with MRS findings in bipolar depression and suggest that inflammatory cytokines may contribute to glutamate alterations in patients with mood disorders and increased inflammation.

In most task and resting state fMRI studies, a group consensus is often sought, where individual variability is considered a nuisance. None the less, biological variability is an important factor that cannot be ignored and is gaining more attention in the field. One recent development is the individual identification based on static functional connectome. While the original work was based on the static connectome, subsequent efforts using recurrent neural networks (RNN) demonstrated that the inclusion of temporal features greatly improved identification accuracy. Given that convolutional RNN (ConvRNN) seamlessly integrates spatial and temporal features, the present work applied ConvRNN for individual identification with resting state fMRI data. Our result demonstrates ConvRNN achieving a higher identification accuracy than conventional RNN, likely due to better extraction of local features between neighboring ROIs. Furthermore, given that each convolutional output assembles in-place features, they provide a natural way for us to visualize the informative spatial pattern and temporal information, opening up a promising new avenue for analyzing fMRI data.

Background: Multi-site functional MRI (fMRI) databases are becoming increasingly prevalent in the study of neurodevelopmental and psychiatric disorders. However, multi-site databases are known to introduce site effects that may confound neurobiological and measures such as functional connectivity (FC). Although studies have been conducted to mitigate site effects, these methods often result in reduced effect size in FC comparisons between controls and patients. Methods: We present a site-wise de-meaning (SWD) strategy in multi-site FC analysis and compare its performance with two common site-effect mitigation methods, i.e., generalized linear model (GLM) and Combining Batches (ComBat) Harmonization. For SWD, after FC was calculated and Fisher z-transformed, the site-wise FC mean was removed from each subject before group-level statistical analysis. The above methods were tested on two multi-site psychiatric consortiums [Autism Brain Imaging Data Exchange (ABIDE) and Bipolar and Schizophrenia Network on Intermediate Phenotypes (B-SNIP)]. Preservation of consistent FC alterations in patients were evaluated for each method through the effect sizes (Hedge’s g) of patients vs. controls. Results: For the B-SNIP dataset, SWD improved the effect size between schizophrenic and control subjects by 4.5–7.9%, while GLM and ComBat decreased the effect size by 22.5–42.6%. For the ABIDE dataset, SWD improved the effect size between autistic and control subjects by 2.9–5.3%, while GLM and ComBat decreased the effect size by up to 11.4%. Conclusion: Compared to the original data and commonly used methods, the SWD method demonstrated superior performance in preserving the effect size in FC features associated with disorders.

Diffusion tensor imaging (DTI) has been used to evaluate white matter (WM) integrity in major depressive disorder (MDD), with several studies reporting differences between depressed patients and controls. However, these findings are variable and taken from relatively small studies often using suboptimal analytic approaches. The presented DTI study examined WM integrity in large samples of medication-free MDD patients (n=134) and healthy controls (n=54) using voxel-based morphometry (VBM) and tract-based spatial statistics (TBSS) approaches, and rigorous statistical thresholds. Compared with health control subjects, MDD patients show no significant differences in fractional anisotropy, radial diffusivity, mean diffusivity, and axonal diffusivity with either the VBM or the TBSS approach. Our findings suggest that disrupted WM integrity does not have a major role in the neurobiology of MDD in this relatively large study using optimal imaging acquisition and analysis; however, this does not eliminate the possibility that certain patient subgroups show WM disruption associated with depression.

The loss of melanized neurons in the substantia nigra pars compacta (SNc) is a hallmark pathology in Parkinson’s disease (PD). Melanized neurons in SNc can be visualized in vivo using magnetization transfer (MT) effects. Nigral volume was extracted in data acquired with a MT-prepared gradient echo sequence in 50 controls, 90 non-manifest carriers (46 LRRK2 and 44 GBA1 nonmanifest carriers), 217 prodromal hyposmic participants, 76 participants with rapid eye movement sleep behavior disorder (RBD), 194 de novo PD patients and 26 moderate PD patients from the Parkinson’s Progressive Markers Initiative. No difference in nigral volume was seen between controls and LRRK2 and GBA1 non-manifest carriers ( F  = 0.732; P  = 0.483). A significant main effect in group was observed between controls, prodromal hyposmic participants, RBD participants, and overt PD patients ( F  = 9.882; P  < 10 −3 ). This study shows that nigral depigmentation can be robustly detected in prodromal and overt PD populations.

A Brain-Computer Interface (BCI) is a setup permitting the control of external devices by decoding brain activity. Electroencephalography (EEG) has been extensively used for decoding brain activity since it is non-invasive, cheap, portable, and has high temporal resolution to allow real-time operation. Due to its poor spatial specificity, BCIs based on EEG can require extensive training and multiple trials to decode brain activity (consequently slowing down the operation of the BCI). On the other hand, BCIs based on functional magnetic resonance imaging (fMRI) are more accurate owing to its superior spatial resolution and sensitivity to underlying neuronal processes which are functionally localized. However, due to its relatively low temporal resolution, high cost, and lack of portability, fMRI is unlikely to be used for routine BCI. We propose a new approach for transferring the capabilities of fMRI to EEG, which includes simultaneous EEG/fMRI sessions for finding a mapping from EEG to fMRI, followed by a BCI run from only EEG data, but driven by fMRI-like features obtained from the mapping identified previously. Our novel data-driven method is likely to discover latent linkages between electrical and hemodynamic signatures of neural activity hitherto unexplored using model-driven methods, and is likely to serve as a template for a novel multi-modal strategy wherein cross-modal EEG-fMRI interactions are exploited for the operation of a unimodal EEG system, leading to a new generation of EEG-based BCIs.