Changes In White Matter Connectivity Research Articles

Association of disruption of the right posterior arcuate fasciculus with spatial neglect.

Spatial neglect is a debilitating condition observed in patients with right-sided brain injuries in whom there is defective awareness of the contralesional space. Although classically considered a right parietal lobe deficit, there has been increasing interest in the specific white matter (WM) architecture subserving spatial neglect. Patients who have lesions associated with chronic disruptions in visuospatial networks are of significant relevance in elucidating the WM tracts associated with spatial attention. In this study, the authors used two independent analytical methods to examine the relationship between WM connectivity changes and spatial attention. Thirty patients with right-sided glioma underwent diffusion tensor imaging (DTI) tractography and neuropsychological testing prior to tumor resection. Spatial neglect was assessed using the Bells Test. Diffusion connectometry analysis was performed to calculate the probability of injury to 55 WM tracts. Next, quantitative DTI tractography was used to reconstruct 9 major WM tracts and obtain fractional anisotropy (FA) and streamline number values as indices of connectivity. Differences in connectivity were assessed between patients with neglect and controls. Of the WM tracts analyzed by diffusion connectometry, only the right posterior segment of the arcuate fasciculus (psAF) showed a higher probability of disconnection in patients with evidence of hemispatial neglect compared to tract reconstructions of previously published healthy controls (hemineglect: 42% ± 12.5%, vs control: 6.3% ± 4.8% [mean ± SEM]; p < 0.05). Of the WM tracts reconstructed by DTI tractography, only the right psAF demonstrated consistently lower indices of connectivity based on the mean streamline number (hemineglect: 550.35 ± 183.41, vs control: 1407.01 ± 319.93; p < 0.05) and FA value (hemineglect: 0.40 ± 0.013, vs control: 0.44 ± 0.0063; p < 0.05) in patients who demonstrated neglect compared to controls. The right long segment of the arcuate fasciculus, inferior frontooccipital fasciculus, and inferior longitudinal fasciculus also demonstrated a lower streamline number, but not a lower FA value, in patients with evidence of hemineglect. These findings suggest that parietotemporal networks mediated by the right psAF may play a critical role in visuospatial attention. This analysis may help to disentangle the organization of the visuospatial attention networks, predict deficits in patients with glioma, and optimize surgical planning.

Posterior white matter integrity and self-reported posterior cortical symptoms using the Colorado Posterior Cortical Questionnaire.

The Colorado Posterior Cortical Questionnaire (CPC-Q) is a self-report, 15-item screening questionnaire for posterior cortical symptoms, including visuospatial and visuoperceptual difficulties. Changes in white matter connectivity may precede obvious gray matter atrophy in neurodegenerative conditions, especially posterior cortical atrophy. Integration of CPC-Q scores and measures of white matter integrity could contribute to earlier detection of posterior cortical syndromes. We investigated the relationships between posterior cortical symptoms as captured by the CPC-Q and diffusion tensor imaging fractional anisotropy (DTI FA) of white matter regions of interest localized to posterior brain regions (posterior thalamic radiations, splenium of corpus callosum, tapetum). Comparisons were also made by diagnostic group [healthy older adult (n = 31), amnestic Alzheimer's disease (AD, n = 18), and posterior cortical atrophy (PCA, n = 9)] and by SENAS battery visuospatial composite score quartile. Exploratory comparisons of all available individual white matter region DTI FA to CPC-Q, as well as comparisons of DTI FA between diagnostic groups and visuospatial quartiles, were also made. CPC-Q score was correlated with the average DTI FA for the averaged posterior white matter regions of interest (r = -0.31, p = 0.02). Posterior thalamic radiation DTI FA was most strongly associated with CPC-Q (r = -0.34, p = 0.01) and visuospatial composite (r = 0.58, p < 0.01) scores and differed between the PCA and AD groups and the lower and higher visuospatial quartiles. The DTI FA of body and splenium of the corpus callosum also demonstrated this pattern but not the DTI FA of the tapetum. The integrity of posterior white matter tracts is associated with scores on the CPC-Q, adding to the validation evidence for this new questionnaire. White matter regions that may be related to posterior cortical symptoms detected by the CPC-Q, and distinct from those affected in amnestic syndromes, include the posterior thalamic radiations and body and splenium of the corpus callosum. These findings are in line with previous neuroimaging studies of PCA and support continued research on white matter in posterior cortical dysfunction.

Discriminative patterns of white matter changes in Alzheimer's

Changes in structural connectivity of the Alzheimer's brain have not been widely studied utilizing cutting-edge methodologies. This study develops an efficient structural connectome-based convolutional neural network (CNN) to classify the AD and uses explanations of CNNs' choices in classification to pinpoint the discriminative changes in white matter connectivity in AD. A CNN architecture has been developed to classify normal control (NC) and AD subjects from the weighted structural connectome. Then, the CNN classification decision is visually analyzed using gradient-based localization techniques to identify the discriminative changes in white matter connectivity in Alzheimer's. The cortical regions involved in the identified discriminative structural connectivity changes in AD are highly covered in the temporal/subcortical regions. A specific pattern is identified in the discriminative changes in structural connectivity of AD, where the white matter changes are revealed within the temporal/subcortical regions and from the temporal/subcortical regions to the frontal and parietal regions in both left and right hemispheres. The proposed approach has the potential to comprehensively analyze the discriminative structural connectivity differences in AD, change the way of detecting biomarkers, and help clinicians better understand the structural changes in AD and provide them with more confidence in automated diagnostic systems.

Changes in the geometry and robustness of diffusion tensor imaging networks: Secondary analysis from a randomized controlled trial of young autistic children receiving an umbilical cord blood infusion.

Diffusion tensor imaging (DTI) has been used as an outcome measure in clinical trials for several psychiatric disorders but has rarely been explored in autism clinical trials. This is despite a large body of research suggesting altered white matter structure in autistic individuals. The current study is a secondary analysis of changes in white matter connectivity from a double-blind placebo-control trial of a single intravenous cord blood infusion in 2-7-year-old autistic children (1). Both clinical assessments and DTI were collected at baseline and 6 months after infusion. This study used two measures of white matter connectivity: change in node-to-node connectivity as measured through DTI streamlines and a novel measure of feedback network connectivity, Ollivier-Ricci curvature (ORC). ORC is a network measure which considers both local and global connectivity to assess the robustness of any given pathway. Using both the streamline and ORC analyses, we found reorganization of white matter pathways in predominantly frontal and temporal brain networks in autistic children who received umbilical cord blood treatment versus those who received a placebo. By looking at changes in network robustness, this study examined not only the direct, physical changes in connectivity, but changes with respect to the whole brain network. Together, these results suggest the use of DTI and ORC should be further explored as a potential biomarker in future autism clinical trials. These results, however, should not be interpreted as evidence for the efficacy of cord blood for improving clinical outcomes in autism. This paper presents a secondary analysis using data from a clinical trial that was prospectively registered with ClinicalTrials.gov(NCT02847182).

Chronic anemia: The effects on the connectivity of white matter.

Chronic anemia is commonly observed in patients with hemoglobinopathies, mainly represented by disorders of altered hemoglobin (Hb) structure (sickle cell disease, SCD) and impaired Hb synthesis (e.g. thalassemia syndromes, non-SCD anemia). Both hemoglobinopathies have been associated with white matter (WM) alterations. Novel structural MRI research in our laboratory demonstrated that WM volume was diffusely lower in deep, watershed areas proportional to anemia severity. Furthermore, diffusion tensor imaging analysis has provided evidence that WM microstructure is disrupted proportionally to Hb level and oxygen saturation. SCD patients have been widely studied and demonstrate lower fractional anisotropy (FA) in the corticospinal tract and cerebellum across the internal capsule and corpus callosum. In the present study, we compared 19 SCD and 15 non-SCD anemia patients with a wide range of Hb values allowing the characterization of the effects of chronic anemia in isolation of sickle Hb. We performed a tensor analysis to quantify FA changes in WM connectivity in chronic anemic patients. We calculated the volumetric mean of FA along the pathway of tracks connecting two regions of interest defined by BrainSuite's BCI-DNI atlas. In general, we found lower FA values in anemic patients; indicating the loss of coherence in the main diffusion direction that potentially indicates WM injury. We saw a positive correlation between FA and hemoglobin in these same regions, suggesting that decreased WM microstructural integrity FA is highly driven by chronic hypoxia. The only connection that did not follow this pattern was the connectivity within the left middle-inferior temporal gyrus. Interestingly, more reductions in FA were observed in non-SCD patients (mainly along with intrahemispheric WM bundles and watershed areas) than the SCD patients (mainly interhemispheric).

Differential Patterns of Change in Brain Connectivity Resulting from Severe Traumatic Brain Injury.

Background: Traumatic brain injury (TBI) damages white matter tracts, disrupting brain network structure and communication. There exists a wide heterogeneity in the pattern of structural damage associated with injury, as well as a large heterogeneity in behavioral outcomes. However, little is known about the relationship between changes in network connectivity and clinical outcomes. Materials and Methods: We utilize the rat lateral fluid-percussion injury model of severe TBI to study differences in brain connectivity in 8 animals that received the insult and 11 animals that received only a craniectomy. Diffusion tensor imaging is performed 5 weeks after the injury and network theory is used to investigate changes in white matter connectivity. Results: We find that (1) global network measures are not able to distinguish between healthy and injured animals; (2) injury induced alterations predominantly exist in a subset of connections (subnetworks) distributed throughout the brain; and (3) injured animals can be divided into subgroups based on changes in network motifs-measures of local structural connectivity. In addition, alterations in predicted functional connectivity indicate that the subgroups have different propensities to synchronize brain activity, which could relate to the heterogeneity of clinical outcomes. Discussion: These results suggest that network measures can be used to quantify progressive changes in brain connectivity due to injury and differentiate among subpopulations with similar injuries, but different pathological trajectories.

Hippocampal subfield imaging and fractional anisotropy show parallel changes in Alzheimer's disease tau progression using simultaneous tau-PET/MRI at 3T.

IntroductionAlzheimer's disease (AD) is the most common form of dementia, characterized primarily by abnormal aggregation of two proteins, tau and amyloid beta. We assessed tau pathology and white matter connectivity changes in subfields of the hippocampus simultaneously in vivo in AD.MethodsTwenty‐four subjects were scanned using simultaneous time‐of‐flight 18F‐PI‐2620 tau positron emission tomography/3‐Tesla magnetic resonance imaging and automated segmentation.ResultsWe observed extensive tau elevation in the entorhinal/perirhinal regions, intermediate tau elevation in cornu ammonis 1/subiculum, and an absence of tau elevation in the dentate gyrus, relative to controls. Diffusion tensor imaging showed parahippocampal gyral fractional anisotropy was lower in AD and mild cognitive impairment compared to controls and strongly correlated with early tau accumulation in the entorhinal and perirhinal cortices.DiscussionThis study demonstrates the potential for quantifiable patterns of 18F‐PI2620 binding in hippocampus subfields, accompanied by diffusion and volume metrics, to be valuable markers of AD.

Auditory and Visual System White Matter Is Differentially Impacted by Normative Aging in Macaques.

Deficits in auditory and visual processing are commonly encountered by older individuals. In addition to the relatively well described age-associated pathologies that reduce sensory processing at the level of the cochlea and eye, multiple changes occur along the ascending auditory and visual pathways that further reduce sensory function in each domain. One fundamental question that remains to be directly addressed is whether the structure and function of the central auditory and visual systems follow similar trajectories across the lifespan or sustain the impacts of brain aging independently. The present study used diffusion magnetic resonance imaging and electrophysiological assessments of auditory and visual system function in adult and aged macaques to better understand how age-related changes in white matter connectivity at multiple levels of each sensory system might impact auditory and visual function. In particular, the fractional anisotropy (FA) of auditory and visual system thalamocortical and interhemispheric corticocortical connections was estimated using probabilistic tractography analyses. Sensory processing and sensory system FA were both reduced in older animals compared with younger adults. Corticocortical FA was significantly reduced only in white matter of the auditory system of aged monkeys, while thalamocortical FA was lower only in visual system white matter of the same animals. Importantly, these structural alterations were significantly associated with sensory function within each domain. Together, these results indicate that age-associated deficits in auditory and visual processing emerge in part from microstructural alterations to specific sensory white matter tracts, and not from general differences in white matter condition across the aging brain.SIGNIFICANCE STATEMENT Age-associated deficits in sensory processing arise from structural and functional alterations to both peripheral sensory organs and central brain regions. It remains unclear whether different sensory systems undergo similar or distinct trajectories in function across the lifespan. To provide novel insights into this question, this study combines electrophysiological assessments of auditory and visual function with diffusion MRI in aged macaques. The results suggest that age-related sensory processing deficits in part result from factors that impact the condition of specific white matter tracts, and not from general decreases in connectivity between sensory brain regions. Such anatomic specificity argues for a framework aimed at understanding vulnerabilities with relatively local influence and brain region specificity.

Robustness of connectome harmonics to local gray matter and long-range white matter connectivity changes

Recently, it has been proposed that the harmonic patterns emerging from the brain's structural connectivity underlie the resting state networks of the human brain. These harmonic patterns, termed connectome harmonics, are estimated as the Laplace eigenfunctions of the combined gray and white matters connectivity matrices and yield a connectome-specific extension of the well-known Fourier basis. However, it remains unclear how topological properties of the combined connectomes constrain the precise shape of the connectome harmonics and their relationships to the resting state networks. Here, we systematically study how alterations of the local and long-range connectivity matrices affect the spatial patterns of connectome harmonics. Specifically, the proportion of local gray matter homogeneous connectivity versus long-range white-matter heterogeneous connectivity is varied by means of weight-based matrix thresholding, distance-based matrix trimming, and several types of matrix randomizations. We demonstrate that the proportion of local gray matter connections plays a crucial role for the emergence of wide-spread, functionally meaningful, and originally published connectome harmonic patterns. This finding is robust for several different cortical surface templates, mesh resolutions, or widths of the local diffusion kernel. Finally, using the connectome harmonic framework, we also provide a proof-of-concept for how targeted structural changes such as the atrophy of inter-hemispheric callosal fibers and gray matter alterations may predict functional deficits associated with neurodegenerative conditions.

White Matter Connectivity in Youth at Risk for Serious Mental Illness: A Longitudinal Analysis

Longitudinal changes in white matter connectivity were assessed in a sample of youth at-risk for serious mental illness (n=183; age 12-25). Diffusion tensor imaging (DTI) was acquired at baseline and 12 months from youth recruited across two sites and classified as healthy controls (n=36), familial risk (n=30), mild-symptoms (n=41), attenuated syndromes (n=70), or transition (n=9) based on clinical assessments. Fractional anisotropy (FA) and mean diffusivity (MD) values were derived for the whole brain white matter, forceps minor, anterior cingulate, anterior thalamic radiations, inferior fronto-occipital fasciculus, superior longitudinal fasciculus, and uncinate fasciculus. MANCOVA analysis controlling for site, sex, and age showed no significant group differences in FA and MD at baseline or at 12 months. Linear mixed effects analysis showed a significant effect for time for most white matter tracts, but no effect for group, or group by time interaction. Transdiagnostic risk groups have similar profiles of WM connectivity and similar rates of change over time.

Amyloid-beta induced retrograde axonal degeneration in a mouse tauopathy model

White matter abnormalities, revealed by Diffusion Tensor Imaging (DTI), are observed in patients with Alzheimer's Disease (AD), representing neural network deficits that underlie gradual cognitive decline in patients. However, how DTI changes related to the development of Amyloid beta (Aβ) and tau pathology, two key hallmarks of AD, remain elusive. We hypothesized that tauopathy induced by Aβ could initiate an axonal degeneration, leading to DTI-detectable white matter abnormalities. We utilized the visual system of the transgenic p301L tau mice as a model system. Aβ was injected in Lateral Geniculate Nucleus (LGN), where the Retinal Ganglion Cell (RGC) axons terminate. Longitudinal DTI was conducted to detect changes in the optic tract (OT) and optic nerve (ON), containing the distal and proximal segments of RGC axons, respectively. Our results showed DTI changes in OT (significant 13.2% reduction in axial diffusion, AxD vs. vehicle controls) followed by significant alterations in ON AxD and fractional anisotropy, FA. Histology data revealed loss of synapses, RGC axons and cell bodies resulting from the Aβ injection. We further tested whether microtubule-stabilizing compound Epothilone D (EpoD) could ameliorate the damage. EpoD co-treatment with Aβ was sufficient to prevent Aβ-induced axon and cell loss. Using an acute injection paradigm, our data suggest that EpoD may mediate its protective effect by blocking localized, acute Aβ-induced tau phosphorylation. This study demonstrates white matter disruption resulting from localized Aβ, the importance of tau pathology induction to changes in white matter connectivity, and the use of EpoD as a potential therapeutic avenue to prevent the axon loss in AD.

Impaired white matter integrity between premotor cortex and basal ganglia in writer's cramp.

IntroductionWriter’s cramp (WC) as a focal hand dystonia is characterized by abnormal postures of the hand during writing. Impaired inhibition and maladaptive plasticity in circuits linking the basal ganglia and sensorimotor cortices have been described. In particular, a dysfunction of lateral premotor cortices has been associated with impaired motor control in WC. We applied diffusion tensor imaging to identify changes in white matter connectivity between premotor regions and important cortical and subcortical structures.MethodsWhole brain white matter tracts were reconstructed in 18 right‐handed WC patients and 18 matched controls, using probabilistic fiber tracking. We restricted our analyses to left‐hemispheric fibers between the middle frontal gyrus (MFG) and basal ganglia, thalamus, primary motor, and sensory cortex. Diffusion parameters (fractional anisotropy and linear anisotropy) were compared between both groups.ResultsA significant reduction in fractional anisotropy values was shown for patients (mean ± SD: 0.37 ± 0.02) vs. controls (0.39 ± 0.03) regarding fibers between the left‐sided MFG and the putamen (p < 0.05). The same applied for linear anisotropy values in this connection (p < 0.05).ConclusionsOur results suggest an impaired structural connectivity between the left‐hemispheric MFG and putamen with a loss of equally aligned fibers in WC patients. This could reflect a structural basis for functional findings interpreted as altered inhibition and plasticity, both within the premotor cortex and the basal ganglia, that at last lead to the clinical symptoms of WC.

Structural brain abnormalities in Cushing's syndrome.

Alongside various physical symptoms, patients with Cushing's disease and Cushing's syndrome display a wide variety of neuropsychiatric and cognitive symptoms, which are indicative of involvement of the central nervous system. The aim of this review is to provide an overview of the structural brain abnormalities that are associated with Cushing's disease and Cushing's syndrome and their relation to behavioral and cognitive symptomatology. In this review, we discuss the gray matter structural abnormalities found in patients with active Cushing's disease and Cushing's syndrome, the reversibility and persistence of these changes and the white matter structural changes related to Cushing's syndrome. Recent findings are of particular interest because they provide more detailed information on localization of the structural changes as well as possible insights into the underlying biological processes. Active Cushing's disease and Cushing's syndrome is related to volume reductions of the hippocampus and in a prefrontal region involving the anterior cingulate cortex (ACC) and medial frontal gyrus (MFG). Whilst there are indications that the reductions in hippocampal volume are partially reversible, the changes in the ACC and MFG appear to be more persistent. In contrast to the volumetric findings, changes in white matter connectivity are typically widespread involving multiple tracts.

Altered white matter connectivity associated with visual hallucinations following occipital stroke

IntroductionVisual hallucinations that arise following vision loss stem from aberrant functional activity in visual cortices and an imbalance of activity across associated cortical and subcortical networks subsequent to visual pathway damage. We sought to determine if structural changes in white matter connectivity play a role in cases of chronic visual hallucinations associated with visual cortical damage.MethodsWe performed diffusion tensor imaging (DTI) and probabilistic fiber tractography to assess white matter connectivity in a patient suffering from continuous and disruptive phosphene (simple) visual hallucinations for more than 2 years following right occipital stroke. We compared these data to that of healthy age‐matched controls.ResultsProbabilistic tractography to reconstruct white matter tracts suggests regeneration of terminal fibers of the ipsilesional optic radiations in the patient. However, arrangement of the converse reconstruction of these tracts, which were seeded from the ipsilesional visual cortex to the intrahemispheric lateral geniculate body, remained disrupted. We further observed compromised structural characteristics, and changes in diffusion (measured using diffusion tensor indices) of white matter tracts in the patient connecting the visual cortex with frontal and temporal regions, and also in interhemispheric connectivity between visual cortices.ConclusionsCortical remapping and the disruption of communication between visual cortices and remote regions are consistent with our previous functional magnetic resonance imaging (fMRI) data showing imbalanced functional activity of the same regions in this patient (Rafique et al, 2016, Neurology, 87, 1493–1500). Long‐term adaptive and disruptive changes in white matter connectivity may account for the rare nature of cases presenting with chronic and continuous visual hallucinations.

White-Matter Pathways for Statistical Learning of Temporal Structures.

Extracting the statistics of event streams in natural environments is critical for interpreting current events and predicting future ones. The brain is known to rapidly find structure and meaning in unfamiliar streams of sensory experience, often by mere exposure to the environment (i.e., without explicit feedback). Yet, we know little about the brain pathways that support this type of statistical learning. Here, we test whether changes in white-matter (WM) connectivity due to training relate to our ability to extract temporal regularities. By combining behavioral training and diffusion tensor imaging (DTI), we demonstrate that humans adapt to the environment’s statistics as they change over time from simple repetition to probabilistic combinations. In particular, we show that learning relates to the decision strategy that individuals adopt when extracting temporal statistics. We next test for learning-dependent changes in WM connectivity and ask whether they relate to individual variability in decision strategy. Our DTI results provide evidence for dissociable WM pathways that relate to individual strategy: extracting the exact sequence statistics (i.e., matching) relates to connectivity changes between caudate and hippocampus, while selecting the most probable outcomes in a given context (i.e., maximizing) relates to connectivity changes between prefrontal, cingulate and basal ganglia (caudate, putamen) regions. Thus, our findings provide evidence for distinct cortico-striatal circuits that show learning-dependent changes of WM connectivity and support individual ability to learn behaviorally-relevant statistics.

A biophysical model of dynamic balancing of excitation and inhibition in fast oscillatory large-scale networks.

Over long timescales, neuronal dynamics can be robust to quite large perturbations, such as changes in white matter connectivity and grey matter structure through processes including learning, aging, development and certain disease processes. One possible explanation is that robust dynamics are facilitated by homeostatic mechanisms that can dynamically rebalance brain networks. In this study, we simulate a cortical brain network using the Wilson-Cowan neural mass model with conduction delays and noise, and use inhibitory synaptic plasticity (ISP) to dynamically achieve a spatially local balance between excitation and inhibition. Using MEG data from 55 subjects we find that ISP enables us to simultaneously achieve high correlation with multiple measures of functional connectivity, including amplitude envelope correlation and phase locking. Further, we find that ISP successfully achieves local E/I balance, and can consistently predict the functional connectivity computed from real MEG data, for a much wider range of model parameters than is possible with a model without ISP.

Changes in structural network are associated with cortical demyelination in early multiple sclerosis.

The aim of this study was to investigate the interplay between structural connectivity and cortical demyelination in early multiple sclerosis. About 27 multiple sclerosis patients and 18 age-matched controls underwent two MRI scanning sessions. The first was done at 7T and involved acquiring quantitative T1 and T2 * high-resolution maps to estimate cortical myelination. The second was done on a Connectom scanner and consisted of acquiring high angular resolution diffusion-weighted images to compute white matter structural connectivity metrics: strength, clustering and local efficiency. To further investigate the interplay between structural connectivity and cortical demyelination, patients were divided into four groups according to disease-duration: 0-1 year, 1-2 years, 2-3 years, and >3 years. ANOVA and Spearman's correlations were used to highlight relations between metrics. ANOVA detected a significant effect between disease duration and both cortical myelin (p = 2 × 10-8 ) and connectivity metrics (p < 10-4 ). We observed significant cortical myelin loss in the shorter disease-duration cohorts (0-1 year, p = .0015), and an increase in connectivity in the longer disease-duration cohort (2-3 years, strength: p = .01, local efficiency: p = .002, clustering: p = .001). Moreover, significant covariations between myelin estimation and white matter connectivity metrics were observed: Spearman's Rho correlation coefficients of 0.52 (p = .0003), 0.55 (p = .0001), and 0.53 (p = .0001) for strength, local efficiency, and clustering, respectively. An association between cortical myelin loss and changes in white matter connectivity in early multiple sclerosis was detected. These changes in network organization might be the result of compensatory mechanisms in response to the ongoing cortical diffuse damage in the early stages of multiple sclerosis.

MRI in the Study of Animal Models of Neurodegenerative Diseases.

Magnetic Resonance Imaging (MRI) is an important tool to study various animal models of degenerative diseases. This chapter describes routine protocols of T 1-, T 2-, and T 2*-weighted and diffusion-weighted MRI for rodentbrain and spinal cord. These protocols can be used to measure atrophy, axonal and myelin injury and changes in white matter connectivity.

Changes in White-Matter Connectivity in Late Second Language Learners: Evidence from Diffusion Tensor Imaging.

Morphological brain changes as a consequence of new learning have been widely established. Learning a second language (L2) is one such experience that can lead to rapid structural neural changes. However, still relatively little is known about how levels of proficiency in the L2 and the age at which the L2 is learned influence brain neuroplasticity. The goal of this study is to provide novel evidence for the effect of bilingualism on white matter structure in relatively proficient but late L2 learners who acquired the second language after early childhood. Overall, the results demonstrate a significant effect on white matter fractional anisotropy (FA) as a function of L2 learning. Higher FA values were found in a broad white matter network including the anterior thalamic radiation (ATR), the inferior fronto-occipital fasciculus (IFOF), the Uncinate Fasciculus (UF), and the inferior longitudinal fasciculus (ILF). Moreover, FA values were correlated with age of L2 acquisition, suggesting that learning an L2, even past childhood, induces neural changes. Finally, these results provide some initial evidence that variability in the age of L2 acquisition has important consequences for neural plasticity.

Changes in functional organization and white matter integrity in the connectome in Parkinson's disease.

Parkinson's disease (PD) leads to dysfunction in multiple cortico-striatal circuits. The neurodegeneration has also been associated with impaired white matter integrity. This structural and functional “disconnection” in PD needs further characterization.We investigated the structural and functional organization of the PD whole brain connectome consisting of 200 nodes using diffusion tensor imaging and resting-state functional MRI, respectively. Data from 20 non-demented PD patients on dopaminergic medication and 20 matched controls were analyzed using graph theory-based methods. We focused on node strength, clustering coefficient, and local efficiency as measures of local network properties; and network modularity as a measure of information flow.PD patients showed reduced white matter connectivity in frontoparietal-striatal nodes compared to controls, but no change in modular organization of the white matter tracts. PD group also showed reduction in functional local network metrics in many nodes distributed across the connectome. There was also decreased functional modularity in the core cognitive networks including the default mode and dorsal attention networks, and sensorimotor network, as well as a lack of modular distinction in the orbitofrontal and basal ganglia nodes in the PD group compared to controls.Our results suggest that despite subtle white matter connectivity changes, the overall structural organization of the PD connectome remains robust at relatively early disease stages. However, there is a breakdown in the functional modular organization of the PD connectome.