2,813 research outputs found
Reduced structural connectivity between left auditory thalamus and the motion-sensitive planum temporale in developmental dyslexia
Developmental dyslexia is characterized by the inability to acquire typical
reading and writing skills. Dyslexia has been frequently linked to cerebral
cortex alterations; however recent evidence also points towards sensory
thalamus dysfunctions: dyslexics showed reduced responses in the left auditory
thalamus (medial geniculate body, MGB) during speech processing in contrast to
neurotypical readers. In addition, in the visual modality, dyslexics have
reduced structural connectivity between the left visual thalamus (lateral
geniculate nucleus, LGN) and V5/MT, a cerebral cortex region involved in visual
movement processing. Higher LGN-V5/MT connectivity in dyslexics was associated
with the faster rapid naming of letters and numbers (RANln), a measure that is
highly correlated with reading proficiency. We here tested two hypotheses that
were directly derived from these previous findings. First, we tested the
hypothesis that dyslexics have reduced structural connectivity between the left
MGB and the auditory motion-sensitive part of the left planum temporale (mPT).
Second, we hypothesized that the amount of left mPT-MGB connectivity correlates
with dyslexics RANln scores. Using diffusion tensor imaging based probabilistic
tracking we show that male adults with developmental dyslexia have reduced
structural connectivity between the left MGB and the left mPT, confirming the
first hypothesis. Stronger left mPT-MGB connectivity was not associated with
faster RANnl scores in dyslexics, but in neurotypical readers. Our findings
provide first evidence that reduced cortico-thalamic connectivity in the
auditory modality is a feature of developmental dyslexia, and that it may also
impact on reading related cognitive abilities in neurotypical readers
Fuzzy Fibers: Uncertainty in dMRI Tractography
Fiber tracking based on diffusion weighted Magnetic Resonance Imaging (dMRI)
allows for noninvasive reconstruction of fiber bundles in the human brain. In
this chapter, we discuss sources of error and uncertainty in this technique,
and review strategies that afford a more reliable interpretation of the
results. This includes methods for computing and rendering probabilistic
tractograms, which estimate precision in the face of measurement noise and
artifacts. However, we also address aspects that have received less attention
so far, such as model selection, partial voluming, and the impact of
parameters, both in preprocessing and in fiber tracking itself. We conclude by
giving impulses for future research
Centralized and distributed cognitive task processing in the human connectome
A key question in modern neuroscience is how cognitive changes in a human
brain can be quantified and captured by functional connectomes (FC) . A
systematic approach to measure pairwise functional distance at different brain
states is lacking. This would provide a straight-forward way to quantify
differences in cognitive processing across tasks; also, it would help in
relating these differences in task-based FCs to the underlying structural
network. Here we propose a framework, based on the concept of Jensen-Shannon
divergence, to map the task-rest connectivity distance between tasks and
resting-state FC. We show how this information theoretical measure allows for
quantifying connectivity changes in distributed and centralized processing in
functional networks. We study resting-state and seven tasks from the Human
Connectome Project dataset to obtain the most distant links across tasks. We
investigate how these changes are associated to different functional brain
networks, and use the proposed measure to infer changes in the information
processing regimes. Furthermore, we show how the FC distance from resting state
is shaped by structural connectivity, and to what extent this relationship
depends on the task. This framework provides a well grounded mathematical
quantification of connectivity changes associated to cognitive processing in
large-scale brain networks.Comment: 22 pages main, 6 pages supplementary, 6 figures, 5 supplementary
figures, 1 table, 1 supplementary table. arXiv admin note: text overlap with
arXiv:1710.0219
Loss of brain inter-frequency hubs in Alzheimer's disease
Alzheimer's disease (AD) causes alterations of brain network structure and
function. The latter consists of connectivity changes between oscillatory
processes at different frequency channels. We proposed a multi-layer network
approach to analyze multiple-frequency brain networks inferred from
magnetoencephalographic recordings during resting-states in AD subjects and
age-matched controls. Main results showed that brain networks tend to
facilitate information propagation across different frequencies, as measured by
the multi-participation coefficient (MPC). However, regional connectivity in AD
subjects was abnormally distributed across frequency bands as compared to
controls, causing significant decreases of MPC. This effect was mainly
localized in association areas and in the cingulate cortex, which acted, in the
healthy group, as a true inter-frequency hub. MPC values significantly
correlated with memory impairment of AD subjects, as measured by the total
recall score. Most predictive regions belonged to components of the
default-mode network that are typically affected by atrophy, metabolism
disruption and amyloid-beta deposition. We evaluated the diagnostic power of
the MPC and we showed that it led to increased classification accuracy (78.39%)
and sensitivity (91.11%). These findings shed new light on the brain functional
alterations underlying AD and provide analytical tools for identifying
multi-frequency neural mechanisms of brain diseases.Comment: 27 pages, 6 figures, 3 tables, 3 supplementary figure
Investigating White Matter Lesion Load, Intrinsic Functional Connectivity, and Cognitive Abilities in Older Adults
Changes to the while matter of the brain disrupt neural communication between spatially distributed brain regions and are associated with cognitive changes in later life. While approximately 95% of older adults experience these brain changes, not everyone who has significant white matter damage displays cognitive impairment. Few studies have investigated the association between white matter changes and cognition in the context of functional brain network integrity. This study used a data-driven, multivariate analytical model to investigate intrinsic functional connectivity patterns associated with individual variability in white matter lesion load as related to fluid and crystallized intelligence in a sample of healthy older adults (n = 84). Several primary findings were noted. First, a reliable pattern emerged associating whole-brain resting-state functional connectivity with individual variability in measures of white matter lesion load, as indexed by total white matter lesion volume and number of lesions. Secondly, white matter lesion load was associated with increased network disintegration and dedifferentiation. Specifically, lower white matter lesion load was associated with greater within- versus between-network connectivity. Higher white matter lesion load was associated with greater between-network connectivity compared to within. These associations between intrinsic functional connectivity and white matter lesion load were not reliably associated with crystallized and fluid intelligence performance. These results suggest that changes to the white matter of the brain in typically aging older adults are characterized by increased functional brain network dedifferentiation. The findings highlight the role of white matter lesion load in altering the functional network architecture of the brain
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