1,281 research outputs found

    Group-wise 3D registration based templates to study the evolution of ant worker neuroanatomy

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    The evolutionary success of ants and other social insects is considered to be intrinsically linked to division of labor and emergent collective intelligence. The role of the brains of individual ants in generating these processes, however, is poorly understood. One genus of ant of special interest is Pheidole, which includes more than a thousand species, most of which are dimorphic, i.e. their colonies contain two subcastes of workers: minors and majors. Using confocal imaging and manual annotations, it has been demonstrated that minor and major workers of different ages of three species of Pheidole have distinct patterns of brain size and subregion scaling. However, these studies require laborious effort to quantify brain region volumes and are subject to potential bias. To address these issues, we propose a group-wise 3D registration approach to build for the first time bias-free brain atlases of intra- and inter-subcaste individuals and automatize the segmentation of new individuals.Comment: 10 pages, 5 figures, preprint for conference (not reviewed

    Geometry Processing of Conventionally Produced Mouse Brain Slice Images

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    Brain mapping research in most neuroanatomical laboratories relies on conventional processing techniques, which often introduce histological artifacts such as tissue tears and tissue loss. In this paper we present techniques and algorithms for automatic registration and 3D reconstruction of conventionally produced mouse brain slices in a standardized atlas space. This is achieved first by constructing a virtual 3D mouse brain model from annotated slices of Allen Reference Atlas (ARA). Virtual re-slicing of the reconstructed model generates ARA-based slice images corresponding to the microscopic images of histological brain sections. These image pairs are aligned using a geometric approach through contour images. Histological artifacts in the microscopic images are detected and removed using Constrained Delaunay Triangulation before performing global alignment. Finally, non-linear registration is performed by solving Laplace's equation with Dirichlet boundary conditions. Our methods provide significant improvements over previously reported registration techniques for the tested slices in 3D space, especially on slices with significant histological artifacts. Further, as an application we count the number of neurons in various anatomical regions using a dataset of 51 microscopic slices from a single mouse brain. This work represents a significant contribution to this subfield of neuroscience as it provides tools to neuroanatomist for analyzing and processing histological data.Comment: 14 pages, 11 figure

    In praise of tedious anatomy

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    Functional neuroimaging is fundamentally a tool for mapping function to structure, and its success consequently requires neuroanatomical precision and accuracy. Here we review the various means by which functional activation can be localized to neuroanatomy and suggest that the gold standard should be localization to the individual’s or group’s own anatomy through the use of neuroanatomical knowledge and atlases of neuroanatomy. While automated means of localization may be useful, they cannot provide the necessary accuracy, given variability between individuals. We also suggest that the field of functional neuroimaging needs to converge on a common set of methods for reporting functional localization including a common “standard” space and criteria for what constitutes sufficient evidence to report activation in terms of Brodmann’s areas

    Neuroimaging of structural pathology and connectomics in traumatic brain injury: Toward personalized outcome prediction.

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    Recent contributions to the body of knowledge on traumatic brain injury (TBI) favor the view that multimodal neuroimaging using structural and functional magnetic resonance imaging (MRI and fMRI, respectively) as well as diffusion tensor imaging (DTI) has excellent potential to identify novel biomarkers and predictors of TBI outcome. This is particularly the case when such methods are appropriately combined with volumetric/morphometric analysis of brain structures and with the exploration of TBI-related changes in brain network properties at the level of the connectome. In this context, our present review summarizes recent developments on the roles of these two techniques in the search for novel structural neuroimaging biomarkers that have TBI outcome prognostication value. The themes being explored cover notable trends in this area of research, including (1) the role of advanced MRI processing methods in the analysis of structural pathology, (2) the use of brain connectomics and network analysis to identify outcome biomarkers, and (3) the application of multivariate statistics to predict outcome using neuroimaging metrics. The goal of the review is to draw the community's attention to these recent advances on TBI outcome prediction methods and to encourage the development of new methodologies whereby structural neuroimaging can be used to identify biomarkers of TBI outcome

    Doctor of Philosophy

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    dissertationNeurodegenerative diseases are an increasing health care problem in the United States. Quantitative neuroimaging provides a noninvasive method to illuminate individual variations in brain structure to better understand and diagnose these disorders. The overall objective of this research is to develop novel clinical tools that summarize and quantify changes in brain shape to not only help better understand age-appropriate changes but also, in the future, to dissociate structural changes associated with aging from those caused by dementing neurodegenerative disorders. Because the tools we will develop can be applied for individual assessment, achieving our goals could have a significant clinical impact. An accurate, practical objective summary measure of the brain pathology would augment current subjective visual interpretation of structural magnetic resonance images. Fractal dimension is a novel approach to image analysis that provides a quantitative measure of shape complexity describing the multiscale folding of the human cerebral cortex. Cerebral cortical folding reflects the complex underlying architectural features that evolve during brain development and degeneration including neuronal density, synaptic proliferation and loss, and gliosis. Building upon existing technology, we have developed innovative tools to compute global and local (voxel-wise and regional) cerebral cortical fractal dimensions and voxel-wise cortico-fractal surfaces from high-contrast MR images. Our previous research has shown that fractal dimension correlates with cognitive function and changes during the course of normal aging. We will now apply unbiased diffeomorphic atlasing methodology to dramatically improve the alignment of complex cortical surfaces. Our novel methods will create more accurate, detailed geometrically averaged images to take into account the intragroup differences and make statistical inferences about spatiotemporal changes in shape of the cerebral cortex across the adult human lifespan

    In Vivo 3D Digital Atlas Database of the Adult C57BL/6J Mouse Brain by Magnetic Resonance Microscopy

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    In this study, a 3D digital atlas of the live mouse brain based on magnetic resonance microscopy (MRM) is presented. C57BL/6J adult mouse brains were imaged in vivo on a 9.4 Tesla MR instrument at an isotropic spatial resolution of 100 μm. With sufficient signal-to-noise (SNR) and contrast-to-noise ratio (CNR), 20 brain regions were identified. Several atlases were constructed including 12 individual brain atlases, an average atlas, a probabilistic atlas and average geometrical deformation maps. We also investigated the feasibility of using lower spatial resolution images to improve time efficiency for future morphological phenotyping. All of the new in vivo data were compared to previous published in vitro C57BL/6J mouse brain atlases and the morphological differences were characterized. Our analyses revealed significant volumetric as well as unexpected geometrical differences between the in vivo and in vitro brain groups which in some instances were predictable (e.g. collapsed and smaller ventricles in vitro) but not in other instances. Based on these findings we conclude that although in vitro datasets, compared to in vivo images, offer higher spatial resolutions, superior SNR and CNR, leading to improved image segmentation, in vivo atlases are likely to be an overall better geometric match for in vivo studies, which are necessary for longitudinal examinations of the same animals and for functional brain activation studies. Thus the new in vivo mouse brain atlas dataset presented here is a valuable complement to the current mouse brain atlas collection and will be accessible to the neuroscience community on our public domain mouse brain atlas website

    Cerebral atrophy in mild cognitive impairment and Alzheimer disease: rates and acceleration.

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    OBJECTIVE: To quantify the regional and global cerebral atrophy rates and assess acceleration rates in healthy controls, subjects with mild cognitive impairment (MCI), and subjects with mild Alzheimer disease (AD). METHODS: Using 0-, 6-, 12-, 18-, 24-, and 36-month MRI scans of controls and subjects with MCI and AD from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database, we calculated volume change of whole brain, hippocampus, and ventricles between all pairs of scans using the boundary shift integral. RESULTS: We found no evidence of acceleration in whole-brain atrophy rates in any group. There was evidence that hippocampal atrophy rates in MCI subjects accelerate by 0.22%/year2 on average (p = 0.037). There was evidence of acceleration in rates of ventricular enlargement in subjects with MCI (p = 0.001) and AD (p < 0.001), with rates estimated to increase by 0.27 mL/year2 (95% confidence interval 0.12, 0.43) and 0.88 mL/year2 (95% confidence interval 0.47, 1.29), respectively. A post hoc analysis suggested that the acceleration of hippocampal loss in MCI subjects was mainly driven by the MCI subjects that were observed to progress to clinical AD within 3 years of baseline, with this group showing hippocampal atrophy rate acceleration of 0.50%/year2 (p = 0.003). CONCLUSIONS: The small acceleration rates suggest a long period of transition to the pathologic losses seen in clinical AD. The acceleration in hippocampal atrophy rates in MCI subjects in the ADNI seems to be driven by those MCI subjects who concurrently progressed to a clinical diagnosis of AD
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