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Hintiryan, Houri, and Hong-Wei Dong. "Brain Networks of Connectionally Unique Basolateral Amygdala Cell Types." Neuroscience Insights 17 (January 2022): 263310552210801. http://dx.doi.org/10.1177/26331055221080175.
Повний текст джерелаАнотація:
Different brain regions structurally interconnected through networks regulate behavior output. Therefore, understanding the functional organization of the brain in health and disease necessitates a foundational anatomic roadmap to its network organization. To provide this to the research community, our lab has systematically traced thousands of pathways in the mouse brain and has applied computational measures to determine the network architecture of major brain systems. Toward this effort, the brain-wide networks of the basolateral amygdalar complex (BLA) were recently generated. The data revealed uniquely connected cell types within the same BLA nucleus that were constituents of distinct neural networks. Here, we elaborate on how these connectionally unique BLA cell types fit within the larger cortico-basal ganglia and limbic networks that were previously described by our team. The significance and utility of high quality, detailed anatomic data is also discussed.
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Scelsi, Marzia Antonella, Valerio Napolioni, Michael D. Greicius, and Andre Altmann. "Network propagation of rare variants in Alzheimer’s disease reveals tissue-specific hub genes and communities." PLOS Computational Biology 17, no. 1 (January 7, 2021): e1008517. http://dx.doi.org/10.1371/journal.pcbi.1008517.
Повний текст джерелаАнотація:
State-of-the-art rare variant association testing methods aggregate the contribution of rare variants in biologically relevant genomic regions to boost statistical power. However, testing single genes separately does not consider the complex interaction landscape of genes, nor the downstream effects of non-synonymous variants on protein structure and function. Here we present the NETwork Propagation-based Assessment of Genetic Events (NETPAGE), an integrative approach aimed at investigating the biological pathways through which rare variation results in complex disease phenotypes. We applied NETPAGE to sporadic, late-onset Alzheimer’s disease (AD), using whole-genome sequencing from the AD Neuroimaging Initiative (ADNI) cohort, as well as whole-exome sequencing from the AD Sequencing Project (ADSP). NETPAGE is based on network propagation, a framework that models information flow on a graph and simulates the percolation of genetic variation through tissue-specific gene interaction networks. The result of network propagation is a set of smoothed gene scores that can be tested for association with disease status through sparse regression. The application of NETPAGE to AD enabled the identification of a set of connected genes whose smoothed variation profile was robustly associated to case-control status, based on gene interactions in the hippocampus. Additionally, smoothed scores significantly correlated with risk of conversion to AD in Mild Cognitive Impairment (MCI) subjects. Lastly, we investigated tissue-specific transcriptional dysregulation of the core genes in two independent RNA-seq datasets, as well as significant enrichments in terms of gene sets with known connections to AD. We present a framework that enables enhanced genetic association testing for a wide range of traits, diseases, and sample sizes.
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Rahman, Hameedur, Tanvir Fatima Naik Bukht, Rozilawati Ahmad, Ahmad Almadhor, and Abdul Rehman Javed. "Efficient Breast Cancer Diagnosis from Complex Mammographic Images Using Deep Convolutional Neural Network." Computational Intelligence and Neuroscience 2023 (March 2, 2023): 1–11. http://dx.doi.org/10.1155/2023/7717712.
Повний текст джерелаАнотація:
Medical image analysis places a significant focus on breast cancer, which poses a significant threat to women’s health and contributes to many fatalities. An early and precise diagnosis of breast cancer through digital mammograms can significantly improve the accuracy of disease detection. Computer-aided diagnosis (CAD) systems must analyze the medical imagery and perform detection, segmentation, and classification processes to assist radiologists with accurately detecting breast lesions. However, early-stage mammography cancer detection is certainly difficult. The deep convolutional neural network has demonstrated exceptional results and is considered a highly effective tool in the field. This study proposes a computational framework for diagnosing breast cancer using a ResNet-50 convolutional neural network to classify mammogram images. To train and classify the INbreast dataset into benign or malignant categories, the framework utilizes transfer learning from the pretrained ResNet-50 CNN on ImageNet. The results revealed that the proposed framework achieved an outstanding classification accuracy of 93%, surpassing other models trained on the same dataset. This novel approach facilitates early diagnosis and classification of malignant and benign breast cancer, potentially saving lives and resources. These outcomes highlight that deep convolutional neural network algorithms can be trained to achieve highly accurate results in various mammograms, along with the capacity to enhance medical tools by reducing the error rate in screening mammograms.
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Torok, Justin, Pedro D. Maia, Parul Verma, Christopher Mezias, and Ashish Raj. "Emergence of directional bias in tau deposition from axonal transport dynamics." PLOS Computational Biology 17, no. 7 (July 27, 2021): e1009258. http://dx.doi.org/10.1371/journal.pcbi.1009258.
Повний текст джерелаАнотація:
Defects in axonal transport may partly underpin the differences between the observed pathophysiology of Alzheimer’s disease (AD) and that of other non-amyloidogenic tauopathies. Particularly, pathological tau variants may have molecular properties that dysregulate motor proteins responsible for the anterograde-directed transport of tau in a disease-specific fashion. Here we develop the first computational model of tau-modified axonal transport that produces directional biases in the spread of tau pathology. We simulated the spatiotemporal profiles of soluble and insoluble tau species in a multicompartment, two-neuron system using biologically plausible parameters and time scales. Changes in the balance of tau transport feedback parameters can elicit anterograde and retrograde biases in the distributions of soluble and insoluble tau between compartments in the system. Aggregation and fragmentation parameters can also perturb this balance, suggesting a complex interplay between these distinct molecular processes. Critically, we show that the model faithfully recreates the characteristic network spread biases in both AD-like and non-AD-like mouse tauopathy models. Tau transport feedback may therefore help link microscopic differences in tau conformational states and the resulting variety in clinical presentations.
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Rezayi, Sorayya, Niloofar Mohammadzadeh, Hamid Bouraghi, Soheila Saeedi, and Ali Mohammadpour. "Timely Diagnosis of Acute Lymphoblastic Leukemia Using Artificial Intelligence-Oriented Deep Learning Methods." Computational Intelligence and Neuroscience 2021 (November 11, 2021): 1–12. http://dx.doi.org/10.1155/2021/5478157.
Повний текст джерелаАнотація:
Background. Leukemia is fatal cancer in both children and adults and is divided into acute and chronic. Acute lymphoblastic leukemia (ALL) is a subtype of this cancer. Early diagnosis of this disease can have a significant impact on the treatment of this disease. Computational intelligence-oriented techniques can be used to help physicians identify and classify ALL rapidly. Materials and Method. In this study, the utilized dataset was collected from a CodaLab competition to classify leukemic cells from normal cells in microscopic images. Two famous deep learning networks, including residual neural network (ResNet-50) and VGG-16 were employed. These two networks are already trained by our assigned parameters, meaning we did not use the stored weights; we adjusted the weights and learning parameters too. Also, a convolutional network with ten convolutional layers and 2 ∗ 2 max-pooling layers—with strides 2—was proposed, and six common machine learning techniques were developed to classify acute lymphoblastic leukemia into two classes. Results. The validation accuracies (the mean accuracy of training and test networks for 100 training cycles) of the ResNet-50, VGG-16, and the proposed convolutional network were found to be 81.63%, 84.62%, and 82.10%, respectively. Among applied machine learning methods, the lowest obtained accuracy was related to multilayer perceptron (27.33%) and highest for random forest (81.72%). Conclusion. This study showed that the proposed convolutional neural network has optimal accuracy in the diagnosis of ALL. By comparing various convolutional neural networks and machine learning methods in diagnosing this disease, the convolutional neural network achieved good performance and optimal execution time without latency. This proposed network is less complex than the two pretrained networks and can be employed by pathologists and physicians in clinical systems for leukemia diagnosis.
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Cheng, Qu, Philip A. Collender, Alexandra K. Heaney, Xintong Li, Rohini Dasan, Charles Li, Joseph A. Lewnard, et al. "The DIOS framework for optimizing infectious disease surveillance: Numerical methods for simulation and multi-objective optimization of surveillance network architectures." PLOS Computational Biology 16, no. 12 (December 4, 2020): e1008477. http://dx.doi.org/10.1371/journal.pcbi.1008477.
Повний текст джерелаАнотація:
Infectious disease surveillance systems provide vital data for guiding disease prevention and control policies, yet the formalization of methods to optimize surveillance networks has largely been overlooked. Decisions surrounding surveillance design parameters—such as the number and placement of surveillance sites, target populations, and case definitions—are often determined by expert opinion or deference to operational considerations, without formal analysis of the influence of design parameters on surveillance objectives. Here we propose a simulation framework to guide evidence-based surveillance network design to better achieve specific surveillance goals with limited resources. We define evidence-based surveillance design as an optimization problem, acknowledging the many operational constraints under which surveillance systems operate, the many dimensions of surveillance system design, the multiple and competing goals of surveillance, and the complex and dynamic nature of disease systems. We describe an analytical framework—the Disease Surveillance Informatics Optimization and Simulation (DIOS) framework—for the identification of optimal surveillance designs through mathematical representations of disease and surveillance processes, definition of objective functions, and numerical optimization. We then apply the framework to the problem of selecting candidate sites to expand an existing surveillance network under alternative objectives of: (1) improving spatial prediction of disease prevalence at unmonitored sites; or (2) estimating the observed effect of a risk factor on disease. Results of this demonstration illustrate how optimal designs are sensitive to both surveillance goals and the underlying spatial pattern of the target disease. The findings affirm the value of designing surveillance systems through quantitative and adaptive analysis of network characteristics and performance. The framework can be applied to the design of surveillance systems tailored to setting-specific disease transmission dynamics and surveillance needs, and can yield improved understanding of tradeoffs between network architectures.
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Haspinger, Daniel Ch, Sandra Klinge, and Gerhard A. Holzapfel. "Numerical analysis of the impact of cytoskeletal actin filament density alterations onto the diffusive vesicle-mediated cell transport." PLOS Computational Biology 17, no. 5 (May 3, 2021): e1008784. http://dx.doi.org/10.1371/journal.pcbi.1008784.
Повний текст джерелаАнотація:
The interior of a eukaryotic cell is a highly complex composite material which consists of water, structural scaffoldings, organelles, and various biomolecular solutes. All these components serve as obstacles that impede the motion of vesicles. Hence, it is hypothesized that any alteration of the cytoskeletal network may directly impact or even disrupt the vesicle transport. A disruption of the vesicle-mediated cell transport is thought to contribute to several severe diseases and disorders, such as diabetes, Parkinson’s and Alzheimer’s disease, emphasizing the clinical relevance. To address the outlined objective, a multiscale finite element model of the diffusive vesicle transport is proposed on the basis of the concept of homogenization, owed to the complexity of the cytoskeletal network. In order to study the microscopic effects of specific nanoscopic actin filament network alterations onto the vesicle transport, a parametrized three-dimensional geometrical model of the actin filament network was generated on the basis of experimentally observed filament densities and network geometries in an adenocarcinomic human alveolar basal epithelial cell. Numerical analyzes of the obtained effective diffusion properties within two-dimensional sampling domains of the whole cell model revealed that the computed homogenized diffusion coefficients can be predicted statistically accurate by a simple two-parameter power law as soon as the inaccessible area fraction, due to the obstacle geometries and the finite size of the vesicles, is known. This relationship, in turn, leads to a massive reduction in computation time and allows to study the impact of a variety of different cytoskeletal alterations onto the vesicle transport. Hence, the numerical simulations predicted a 35% increase in transport time due to a uniformly distributed four-fold increase of the total filament amount. On the other hand, a hypothetically reduced expression of filament cross-linking proteins led to sparser filament networks and, thus, a speed up of the vesicle transport.
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Jansen, Joanneke E., Dominik Aschenbrenner, Holm H. Uhlig, Mark C. Coles, and Eamonn A. Gaffney. "A method for the inference of cytokine interaction networks." PLOS Computational Biology 18, no. 6 (June 22, 2022): e1010112. http://dx.doi.org/10.1371/journal.pcbi.1010112.
Повний текст джерелаАнотація:
Cell-cell communication is mediated by many soluble mediators, including over 40 cytokines. Cytokines, e.g. TNF, IL1β, IL5, IL6, IL12 and IL23, represent important therapeutic targets in immune-mediated inflammatory diseases (IMIDs), such as inflammatory bowel disease (IBD), psoriasis, asthma, rheumatoid and juvenile arthritis. The identification of cytokines that are causative drivers of, and not just associated with, inflammation is fundamental for selecting therapeutic targets that should be studied in clinical trials. As in vitro models of cytokine interactions provide a simplified framework to study complex in vivo interactions, and can easily be perturbed experimentally, they are key for identifying such targets. We present a method to extract a minimal, weighted cytokine interaction network, given in vitro data on the effects of the blockage of single cytokine receptors on the secretion rate of other cytokines. Existing biological network inference methods typically consider the correlation structure of the underlying dataset, but this can make them poorly suited for highly connected, non-linear cytokine interaction data. Our method uses ordinary differential equation systems to represent cytokine interactions, and efficiently computes the configuration with the lowest Akaike information criterion value for all possible network configurations. It enables us to study indirect cytokine interactions and quantify inhibition effects. The extracted network can also be used to predict the combined effects of inhibiting various cytokines simultaneously. The model equations can easily be adjusted to incorporate more complicated dynamics and accommodate temporal data. We validate our method using synthetic datasets and apply our method to an experimental dataset on the regulation of IL23, a cytokine with therapeutic relevance in psoriasis and IBD. We validate several model predictions against experimental data that were not used for model fitting. In summary, we present a novel method specifically designed to efficiently infer cytokine interaction networks from cytokine perturbation data in the context of IMIDs.
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Corriveau-Lecavalier, Nick, Jeffrey L. Gunter, Michael Kamykowski, Ellen Dicks, Hugo Botha, Walter K. Kremers, Jonathan Graff-Radford, et al. "Default mode network failure and neurodegeneration across aging and amnestic and dysexecutive Alzheimer’s disease." Brain Communications, March 8, 2023. http://dx.doi.org/10.1093/braincomms/fcad058.
Повний текст джерелаАнотація:
Abstract From a complex systems perspective, clinical syndromes emerging from neurodegenerative diseases are thought to result from multiscale interactions between aggregates of misfolded proteins and the disequilibrium of large-scale networks coordinating functional operations underpinning cognitive phenomena. Across all syndromic presentations of Alzheimer’s disease, age-related disruption of the default mode network is accelerated by amyloid deposition. Conversely, syndromic variability may reflect selective neurodegeneration of modular networks supporting specific cognitive abilities. In this study, we leveraged the breadth of the Human Connectome Project-Aging cohort of non-demented individuals (N = 724) as a normative cohort to assess the robustness of a biomarker of default mode network dysfunction in Alzheimer’s disease, the network failure quotient, across the aging spectrum. We then examined the capacity of the network failure quotient and focal markers of neurodegeneration to discriminate patients with amnestic (N = 8) or dysexecutive (N = 10) Alzheimer’s disease from the normative cohort at the patient-level, as well as between Alzheimer’s disease phenotypes. Importantly, all participants and patients were scanned using the Human Connectome Project-Aging protocol, allowing for the acquisition of high-resolution structural imaging and longer resting-state connectivity acquisition time. Using a regression framework, we found that the network failure quotient related to age, global and focal cortical thickness, hippocampal volume, and cognition in the normative Human Connectome Project-Aging cohort, replicating previous results from the Mayo Clinic Study of Aging that used a different scanning protocol. Then, we used quantile curves and group-wise comparisons to show that the network failure quotient commonly distinguished both dysexecutive and amnestic Alzheimer’s disease patients from the normative cohort. In contrast, focal neurodegeneration markers were more phenotype-specific, where the neurodegeneration of parieto-frontal areas associated with dysexecutive Alzheimer’s disease while the neurodegeneration of hippocampal and temporal areas associated with amnestic Alzheimer’s disease. Capitalizing on a large normative cohort and optimized imaging acquisition protocols, we highlight a biomarker of default mode network failure reflecting shared system-level pathophysiological mechanisms across aging and dysexecutive and amnestic Alzheimer’s disease and biomarkers of focal neurodegeneration reflecting distinct pathognomonic processes across the amnestic and dysexecutive Alzheimer’s disease phenotypes. These findings provide evidence that variability in inter-individual cognitive impairment in Alzheimer’s disease may relate to both modular network degeneration and default mode network disruption. These results provide important information to advance complex systems approaches to cognitive aging and degeneration, expand the armamentarium of biomarkers available to aid diagnosis, monitor progression, and inform clinical trials.
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Pena, Danilo, Jessika Suescun, Mya Schiess, Timothy M. Ellmore, and Luca Giancardo. "Toward a Multimodal Computer-Aided Diagnostic Tool for Alzheimer’s Disease Conversion." Frontiers in Neuroscience 15 (January 3, 2022). http://dx.doi.org/10.3389/fnins.2021.744190.
Повний текст джерелаАнотація:
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder. It is one of the leading sources of morbidity and mortality in the aging population AD cardinal symptoms include memory and executive function impairment that profoundly alters a patient’s ability to perform activities of daily living. People with mild cognitive impairment (MCI) exhibit many of the early clinical symptoms of patients with AD and have a high chance of converting to AD in their lifetime. Diagnostic criteria rely on clinical assessment and brain magnetic resonance imaging (MRI). Many groups are working to help automate this process to improve the clinical workflow. Current computational approaches are focused on predicting whether or not a subject with MCI will convert to AD in the future. To our knowledge, limited attention has been given to the development of automated computer-assisted diagnosis (CAD) systems able to provide an AD conversion diagnosis in MCI patient cohorts followed longitudinally. This is important as these CAD systems could be used by primary care providers to monitor patients with MCI. The method outlined in this paper addresses this gap and presents a computationally efficient pre-processing and prediction pipeline, and is designed for recognizing patterns associated with AD conversion. We propose a new approach that leverages longitudinal data that can be easily acquired in a clinical setting (e.g., T1-weighted magnetic resonance images, cognitive tests, and demographic information) to identify the AD conversion point in MCI subjects with AUC = 84.7. In contrast, cognitive tests and demographics alone achieved AUC = 80.6, a statistically significant difference (n = 669, p < 0.05). We designed a convolutional neural network that is computationally efficient and requires only linear registration between imaging time points. The model architecture combines Attention and Inception architectures while utilizing both cross-sectional and longitudinal imaging and clinical information. Additionally, the top brain regions and clinical features that drove the model’s decision were investigated. These included the thalamus, caudate, planum temporale, and the Rey Auditory Verbal Learning Test. We believe our method could be easily translated into the healthcare setting as an objective AD diagnostic tool for patients with MCI.
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Hwang, Eun Jung, Takashi R. Sato, and Tatsuo K. Sato. "A Canonical Scheme of Bottom-Up and Top-Down Information Flows in the Frontoparietal Network." Frontiers in Neural Circuits 15 (August 12, 2021). http://dx.doi.org/10.3389/fncir.2021.691314.
Повний текст джерелаАнотація:
Goal-directed behavior often involves temporal separation and flexible context-dependent association between sensory input and motor output. The control of goal-directed behavior is proposed to lie in the frontoparietal network, but the computational architecture of this network remains elusive. Based on recent rodent studies that measured and manipulated projection neurons in the frontoparietal network together with findings from earlier primate studies, we propose a canonical scheme of information flows in this network. The parietofrontal pathway transmits the spatial information of a sensory stimulus or internal motor bias to drive motor programs in the frontal areas. This pathway might consist of multiple parallel connections, each controlling distinct motor effectors. The frontoparietal pathway sends the spatial information of cognitively processed motor plans through multiple parallel connections. Each of these connections could support distinct spatial functions that use the motor target information, including attention allocation, multi-body part coordination, and forward estimation of movement state (i.e., forward models). The parallel pathways in the frontoparietal network enable dynamic interactions between regions that are tuned for specific goal-directed behaviors. This scheme offers a promising framework within which the computational architecture of the frontoparietal network and the underlying circuit mechanisms can be delineated in a systematic way, providing a holistic understanding of information processing in this network. Clarifying this network may also improve the diagnosis and treatment of behavioral deficits associated with dysfunctional frontoparietal connectivity in various neurological disorders including Alzheimer’s disease.
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Chang, Ya-Ting, Shih-Wei Hsu, Shu-Hua Huang, Chi-Wei Huang, Wen-Neng Chang, Chia-Yi Lien, Jun-Jun Lee, Chen-Chang Lee та Chiung-Chih Chang. "ABCA7 polymorphisms correlate with memory impairment and default mode network in patients with APOEε4-associated Alzheimer’s disease". Alzheimer's Research & Therapy 11, № 1 (грудень 2019). http://dx.doi.org/10.1186/s13195-019-0563-3.
Повний текст джерелаАнотація:
Abstract Background Since both APOE and ABCA7 protein expression may independently reduce neuritic plaque burden and reorganize fibrillar amyloid burden-mediated disruption of functional connectivity in the default mode network, we aimed to investigate the effect of the APOE-ABCA7 interaction on default mode network in Alzheimer’s disease. Methods Two hundred and eighty-seven individuals with a diagnosis of typical Alzheimer’s disease were included in this study. Memory was characterized and compared between APOE-ε4+ carriers and APOE-ε4 non-carriers within ABCA7 rs3764650T allele homozygous carriers and ABCA7 rs3764650G allele carriers, respectively. Two-way analysis of variance was used to identify a significant interaction effect between APOE (APOE-ε4+ carriers versus APOE-ε4 non-carriers) and ABCA7 (ABCA7 rs3764650T allele homozygous versus ABCA7 rs3764650G allele carriers) on memory scores and functional connectivity in each default mode network subsystem. Results In ABCA7 rs3764650G allele carriers, APOE-ε4+ carriers had lower memory scores (t (159) = − 4.879; P < 0.001) compared to APOE-ε4 non-carriers, but APOE-ε4+ carriers and APOE-ε4 non-carriers did not have differences in memory (P > 0.05) within ABCA7 rs3764650T allele homozygous carriers. There was a significant APOE-ABCA7 interaction effect on the memory (F3, 283 = 4.755, P = 0.030). In the default mode network anchored by the entorhinal seed, the peak neural activity of the cluster that was significantly associated with APOE-ABCA7 interaction effects (P = 0.00002) was correlated with the memory (ρ = 0.129, P = 0.030). Conclusions Genetic-biological systems may impact disease presentation and therapy. Clarifying the effect of APOE-ABCA7 interactions on the default mode network and memory is critical to exploring the complex pathogenesis of Alzheimer’s disease and refining a potential therapy.
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Griguoli, Marilena, and Domenico Pimpinella. "Medial septum: relevance for social memory." Frontiers in Neural Circuits 16 (August 23, 2022). http://dx.doi.org/10.3389/fncir.2022.965172.
Повний текст джерелаАнотація:
Animal species are named social when they develop the capability of complex behaviors based on interactions with conspecifics that include communication, aggression, mating and parental behavior, crucial for well-being and survival. The underpinning of such complex behaviors is social memory, namely the capacity to discriminate between familiar and novel individuals. The Medial Septum (MS), a region localized in the basal forebrain, is part of the brain network involved in social memory formation. MS receives several cortical and subcortical synaptic and neuromodulatory inputs that make it an important hub in processing social information relevant for social memory. Particular attention is paid to synaptic inputs that control both the MS and the CA2 region of the hippocampus, one of the major MS output, that has been causally linked to social memory. In this review article, we will provide an overview of local and long range connectivity that allows MS to integrate and process social information. Furthermore, we will summarize previous strategies used to determine how MS controls social memory in different animal species. Finally, we will discuss the impact of an altered MS signaling on social memory in animal models and patients affected by neurodevelopmental and neurodegenerative disorders, including autism and Alzheimer’s Disease.
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Honoré, Eve, Abdessattar Khlaifia, Anthony Bosson, and Jean-Claude Lacaille. "Hippocampal Somatostatin Interneurons, Long-Term Synaptic Plasticity and Memory." Frontiers in Neural Circuits 15 (June 2, 2021). http://dx.doi.org/10.3389/fncir.2021.687558.
Повний текст джерелаАнотація:
A distinctive feature of the hippocampal structure is the diversity of inhibitory interneurons. These complex inhibitory interconnections largely contribute to the tight modulation of hippocampal circuitry, as well as to the formation and coordination of neuronal assemblies underlying learning and memory. Inhibitory interneurons provide more than a simple transitory inhibition of hippocampal principal cells (PCs). The synaptic plasticity of inhibitory neurons provides long-lasting changes in the hippocampal network and is a key component of memory formation. The dendrite targeting interneurons expressing the peptide somatostatin (SOM) are particularly interesting in this regard because they display unique long-lasting synaptic changes leading to metaplastic regulation of hippocampal networks. In this article, we examine the actions of the neuropeptide SOM on hippocampal cells, synaptic plasticity, learning, and memory. We address the different subtypes of hippocampal SOM interneurons. We describe the long-term synaptic plasticity that takes place at the excitatory synapses of SOM interneurons, its singular induction and expression mechanisms, as well as the consequences of these changes on the hippocampal network, learning, and memory. We also review evidence that astrocytes provide cell-specific dynamic regulation of inhibition of PC dendrites by SOM interneurons. Finally, we cover how, in mouse models of Alzheimer’s disease (AD), dysfunction of plasticity of SOM interneuron excitatory synapses may also contribute to cognitive impairments in brain disorders.
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Albers, Jasper, Jari Pronold, Anno Christopher Kurth, Stine Brekke Vennemo, Kaveh Haghighi Mood, Alexander Patronis, Dennis Terhorst, et al. "A Modular Workflow for Performance Benchmarking of Neuronal Network Simulations." Frontiers in Neuroinformatics 16 (May 11, 2022). http://dx.doi.org/10.3389/fninf.2022.837549.
Повний текст джерелаАнотація:
Modern computational neuroscience strives to develop complex network models to explain dynamics and function of brains in health and disease. This process goes hand in hand with advancements in the theory of neuronal networks and increasing availability of detailed anatomical data on brain connectivity. Large-scale models that study interactions between multiple brain areas with intricate connectivity and investigate phenomena on long time scales such as system-level learning require progress in simulation speed. The corresponding development of state-of-the-art simulation engines relies on information provided by benchmark simulations which assess the time-to-solution for scientifically relevant, complementary network models using various combinations of hardware and software revisions. However, maintaining comparability of benchmark results is difficult due to a lack of standardized specifications for measuring the scaling performance of simulators on high-performance computing (HPC) systems. Motivated by the challenging complexity of benchmarking, we define a generic workflow that decomposes the endeavor into unique segments consisting of separate modules. As a reference implementation for the conceptual workflow, we develop beNNch: an open-source software framework for the configuration, execution, and analysis of benchmarks for neuronal network simulations. The framework records benchmarking data and metadata in a unified way to foster reproducibility. For illustration, we measure the performance of various versions of the NEST simulator across network models with different levels of complexity on a contemporary HPC system, demonstrating how performance bottlenecks can be identified, ultimately guiding the development toward more efficient simulation technology.
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Di Paolo, Andres, Joaquin Garat, Guillermo Eastman, Joaquina Farias, Federico Dajas-Bailador, Pablo Smircich, and José Roberto Sotelo-Silveira. "Functional Genomics of Axons and Synapses to Understand Neurodegenerative Diseases." Frontiers in Cellular Neuroscience 15 (June 25, 2021). http://dx.doi.org/10.3389/fncel.2021.686722.
Повний текст джерелаАнотація:
Functional genomics studies through transcriptomics, translatomics and proteomics have become increasingly important tools to understand the molecular basis of biological systems in the last decade. In most cases, when these approaches are applied to the nervous system, they are centered in cell bodies or somatodendritic compartments, as these are easier to isolate and, at least in vitro, contain most of the mRNA and proteins present in all neuronal compartments. However, key functional processes and many neuronal disorders are initiated by changes occurring far away from cell bodies, particularly in axons (axopathologies) and synapses (synaptopathies). Both neuronal compartments contain specific RNAs and proteins, which are known to vary depending on their anatomical distribution, developmental stage and function, and thus form the complex network of molecular pathways required for neuron connectivity. Modifications in these components due to metabolic, environmental, and/or genetic issues could trigger or exacerbate a neuronal disease. For this reason, detailed profiling and functional understanding of the precise changes in these compartments may thus yield new insights into the still intractable molecular basis of most neuronal disorders. In the case of synaptic dysfunctions or synaptopathies, they contribute to dozens of diseases in the human brain including neurodevelopmental (i.e., autism, Down syndrome, and epilepsy) as well as neurodegenerative disorders (i.e., Alzheimer’s and Parkinson’s diseases). Histological, biochemical, cellular, and general molecular biology techniques have been key in understanding these pathologies. Now, the growing number of omics approaches can add significant extra information at a high and wide resolution level and, used effectively, can lead to novel and insightful interpretations of the biological processes at play. This review describes current approaches that use transcriptomics, translatomics and proteomic related methods to analyze the axon and presynaptic elements, focusing on the relationship that axon and synapses have with neurodegenerative diseases.
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Corcoran, Carl, and Alan Hastings. "A Low-Dimensional Network Model for an SIS Epidemic: Analysis of the Super Compact Pairwise Model." Bulletin of Mathematical Biology 83, no. 7 (May 21, 2021). http://dx.doi.org/10.1007/s11538-021-00907-2.
Повний текст джерелаАнотація:
AbstractNetwork-based models of epidemic spread have become increasingly popular in recent decades. Despite a rich foundation of such models, few low-dimensional systems for modeling SIS-type diseases have been proposed that manage to capture the complex dynamics induced by the network structure. We analyze one recently introduced model and derive important epidemiological quantities for the system. We derive the epidemic threshold and analyze the bifurcation that occurs, and we use asymptotic techniques to derive an approximation for the endemic equilibrium when it exists. We consider the sensitivity of this approximation to network parameters, and the implications for disease control measures are found to be in line with the results of existing studies.