Relevant bibliographies by topics / Neurodegenerative disease modeling

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Neurodegenerative disease modeling'

Author: Grafiati
Published: 25 May 2024

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Journal articles on the topic "Neurodegenerative disease modeling"

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Bolus, Harris, Kassi Crocker, Grace Boekhoff-Falk, and Stanislava Chtarbanova. "Modeling Neurodegenerative Disorders in Drosophila melanogaster." International Journal of Molecular Sciences 21, no. 9 (April 26, 2020): 3055. http://dx.doi.org/10.3390/ijms21093055.

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Drosophila melanogaster provides a powerful genetic model system in which to investigate the molecular mechanisms underlying neurodegenerative diseases. In this review, we discuss recent progress in Drosophila modeling Alzheimer’s Disease, Parkinson’s Disease, Amyotrophic Lateral Sclerosis (ALS), Huntington’s Disease, Ataxia Telangiectasia, and neurodegeneration related to mitochondrial dysfunction or traumatic brain injury. We close by discussing recent progress using Drosophila models of neural regeneration and how these are likely to provide critical insights into future treatments for neurodegenerative disorders.
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Caldwell, Kim A., Corey W. Willicott, and Guy A. Caldwell. "Modeling neurodegeneration in Caenorhabditiselegans." Disease Models & Mechanisms 13, no. 10 (October 1, 2020): dmm046110. http://dx.doi.org/10.1242/dmm.046110.

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ABSTRACTThe global burden of neurodegenerative diseases underscores the urgent need for innovative strategies to define new drug targets and disease-modifying factors. The nematode Caenorhabditis elegans has served as the experimental subject for multiple transformative discoveries that have redefined our understanding of biology for ∼60 years. More recently, the considerable attributes of C. elegans have been applied to neurodegenerative diseases, including amyotrophic lateral sclerosis, Alzheimer's disease, Parkinson's disease and Huntington's disease. Transgenic nematodes with genes encoding normal and disease variants of proteins at the single- or multi-copy level under neuronal-specific promoters limits expression to select neuronal subtypes. The anatomical transparency of C. elegans affords the use of co-expressed fluorescent proteins to follow the progression of neurodegeneration as the animals age. Significantly, a completely defined connectome facilitates detailed understanding of the impact of neurodegeneration on organismal health and offers a unique capacity to accurately link cell death with behavioral dysfunction or phenotypic variation in vivo. Moreover, chemical treatments, as well as forward and reverse genetic screening, hasten the identification of modifiers that alter neurodegeneration. When combined, these chemical-genetic analyses establish critical threshold states to enhance or reduce cellular stress for dissecting associated pathways. Furthermore, C. elegans can rapidly reveal whether lifespan or healthspan factor into neurodegenerative processes. Here, we outline the methodologies employed to investigate neurodegeneration in C. elegans and highlight numerous studies that exemplify its utility as a pre-clinical intermediary to expedite and inform mammalian translational research.
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Li, Jonathan, and Ernest Fraenkel. "Phenotyping Neurodegeneration in Human iPSCs." Annual Review of Biomedical Data Science 4, no. 1 (July 20, 2021): 83–100. http://dx.doi.org/10.1146/annurev-biodatasci-092820-025214.

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Induced pluripotent stem cell (iPSC) technology holds promise for modeling neurodegenerative diseases. Traditional approaches for disease modeling using animal and cellular models require knowledge of disease mutations. However, many patients with neurodegenerative diseases do not have a known genetic cause. iPSCs offer a way to generate patient-specific models and study pathways of dysfunction in an in vitro setting in order to understand the causes and subtypes of neurodegeneration. Furthermore, iPSC-based models can be used to search for candidate therapeutics using high-throughput screening. Here we review how iPSC-based models are currently being used to further our understanding of neurodegenerative diseases, as well as discuss their challenges and future directions.
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Lepesant, Jean-Antoine. "The promises of neurodegenerative disease modeling." Comptes Rendus Biologies 338, no. 8-9 (August 2015): 584–92. http://dx.doi.org/10.1016/j.crvi.2015.06.018.

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Louit, Aurélie, Todd Galbraith, and François Berthod. "In Vitro 3D Modeling of Neurodegenerative Diseases." Bioengineering 10, no. 1 (January 10, 2023): 93. http://dx.doi.org/10.3390/bioengineering10010093.

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The study of neurodegenerative diseases (such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, or amyotrophic lateral sclerosis) is very complex due to the difficulty in investigating the cellular dynamics within nervous tissue. Despite numerous advances in the in vivo study of these diseases, the use of in vitro analyses is proving to be a valuable tool to better understand the mechanisms implicated in these diseases. Although neural cells remain difficult to obtain from patient tissues, access to induced multipotent stem cell production now makes it possible to generate virtually all neural cells involved in these diseases (from neurons to glial cells). Many original 3D culture model approaches are currently being developed (using these different cell types together) to closely mimic degenerative nervous tissue environments. The aim of these approaches is to allow an interaction between glial cells and neurons, which reproduces pathophysiological reality by co-culturing them in structures that recapitulate embryonic development or facilitate axonal migration, local molecule exchange, and myelination (to name a few). This review details the advantages and disadvantages of techniques using scaffolds, spheroids, organoids, 3D bioprinting, microfluidic systems, and organ-on-a-chip strategies to model neurodegenerative diseases.
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Leventoux, Nicolas, Satoru Morimoto, Kent Imaizumi, Yuta Sato, Shinichi Takahashi, Kyoko Mashima, Mitsuru Ishikawa, et al. "Human Astrocytes Model Derived from Induced Pluripotent Stem Cells." Cells 9, no. 12 (December 13, 2020): 2680. http://dx.doi.org/10.3390/cells9122680.

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Induced pluripotent stem cell (iPSC)-based disease modeling has a great potential for uncovering the mechanisms of pathogenesis, especially in the case of neurodegenerative diseases where disease-susceptible cells can usually not be obtained from patients. So far, the iPSC-based modeling of neurodegenerative diseases has mainly focused on neurons because the protocols for generating astrocytes from iPSCs have not been fully established. The growing evidence of astrocytes’ contribution to neurodegenerative diseases has underscored the lack of iPSC-derived astrocyte models. In the present study, we established a protocol to efficiently generate iPSC-derived astrocytes (iPasts), which were further characterized by RNA and protein expression profiles as well as functional assays. iPasts exhibited calcium dynamics and glutamate uptake activity comparable to human primary astrocytes. Moreover, when co-cultured with neurons, iPasts enhanced neuronal synaptic maturation. Our protocol can be used for modeling astrocyte-related disease phenotypes in vitro and further exploring the contribution of astrocytes to neurodegenerative diseases.
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Li, Bang, Da-Jian He, Xiao-Jiang Li, and Xiang-Yu Guo. "Modeling neurodegenerative diseases using non-human primates: advances and challenges." Ageing and Neurodegenerative Diseases 2, no. 3 (2022): 12. http://dx.doi.org/10.20517/and.2022.14.

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Neurodegenerative diseases (NDs), such as Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), and amyotrophic lateral sclerosis (ALS), are pathologically characterized by progressive loss of selective populations of neurons in the affected brain regions and clinically manifested by cognitive, motor, and psychological dysfunctions. Since aging is the major risk factor for NDs and the elderly population is expected to expand considerably in the coming decades, the prevalence of NDs will significantly increase, leading to a greater medical burden to society and affected families. Despite extensive research on NDs, no effective therapy is available for NDs, largely due to a lack of complete understanding of the pathogenesis of NDs. Although research on small animal and rodent models has provided tremendous knowledge of molecular mechanisms of disease pathogenesis, few translational successes have been reported in clinical trials. In particular, most genetically modified rodent models are unable to recapitulate striking and overt neurodegeneration seen in the patient brains. Non-human primates (NHPs) are the most relevant laboratory animals to humans, and recent studies using NHP neurodegeneration models have uncovered important pathological features of NDs. Here, we review the unique features of NHPs for modeling NDs and new insights into AD, PD, and ALS gained from animal models, highlight the contribution of gene editing techniques to establishing NHP models, and discuss the challenges of investigating NHP models.
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Trudler, Dorit, Swagata Ghatak, and Stuart A. Lipton. "Emerging hiPSC Models for Drug Discovery in Neurodegenerative Diseases." International Journal of Molecular Sciences 22, no. 15 (July 30, 2021): 8196. http://dx.doi.org/10.3390/ijms22158196.

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Neurodegenerative diseases affect millions of people worldwide and are characterized by the chronic and progressive deterioration of neural function. Neurodegenerative diseases, such as Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), and Huntington’s disease (HD), represent a huge social and economic burden due to increasing prevalence in our aging society, severity of symptoms, and lack of effective disease-modifying therapies. This lack of effective treatments is partly due to a lack of reliable models. Modeling neurodegenerative diseases is difficult because of poor access to human samples (restricted in general to postmortem tissue) and limited knowledge of disease mechanisms in a human context. Animal models play an instrumental role in understanding these diseases but fail to comprehensively represent the full extent of disease due to critical differences between humans and other mammals. The advent of human-induced pluripotent stem cell (hiPSC) technology presents an advantageous system that complements animal models of neurodegenerative diseases. Coupled with advances in gene-editing technologies, hiPSC-derived neural cells from patients and healthy donors now allow disease modeling using human samples that can be used for drug discovery.
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Haider, Mohamad, Anjali Chauhan, Sana Tariq, Dharam Pal Pathak, Nadeem Siddiqui, Soni Ali, Faheem Hyder Pottoo, and Ruhi Ali. "Application of In silico Methods in the Design of Drugs for Neurodegenerative Diseases." Current Topics in Medicinal Chemistry 21, no. 11 (August 4, 2021): 995–1011. http://dx.doi.org/10.2174/1568026621666210521164545.

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Neurodegenerative diseases are complex disorders that cause neuron loss, brain aging and ultimately lead to death. These diseases are difficult to treat because of the complex nature of the nervous system, and the available medicines are unable to heal them effectively. This fact implies the need for novel therapeutics to be designed that are ready to stop or a minimum of retard the neurodegeneration process. These days, Computer-Assisted Drug Design (CADD) approaches are a passage to extend the drug development efficiency and to reduce time and cost because traditional drug discovery is both time-consuming as well as costly. Computational or in silico methods came up with powerful tools in drug design against neurodegenerative diseases. This review presents the approaches and theoretical basis of CADD. Also, the successful applications of various in silico studies, including homology modeling, molecular docking, Quantitative Structure-Activity Relationship (QSAR), Molecular Dynamic (MD), De novo drug design, Pharmacophore-based drug design, Virtual Screening (VS), LIGPLOT Analysis, In silico ADMET and drug safety prediction, for treating neurodegenerative diseases have also been included in this review. Major emphasis is given to Alzheimer’s disease and Parkinson’s disease because these two are the most familiar neurodegenerative diseases.
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Wan, Wenbin, Lan Cao, Bill Kalionis, Shijin Xia, and Xiantao Tai. "Applications of Induced Pluripotent Stem Cells in Studying the Neurodegenerative Diseases." Stem Cells International 2015 (2015): 1–11. http://dx.doi.org/10.1155/2015/382530.

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Neurodegeneration is the umbrella term for the progressive loss of structure or function of neurons. Incurable neurodegenerative disorders such as Alzheimer’s disease (AD) and Parkinson’s disease (PD) show dramatic rising trends particularly in the advanced age groups. However, the underlying mechanisms are not yet fully elucidated, and to date there are no biomarkers for early detection or effective treatments for the underlying causes of these diseases. Furthermore, due to species variation and differences between animal models (e.g., mouse transgenic and knockout models) of neurodegenerative diseases, substantial debate focuses on whether animal and cell culture disease models can correctly model the condition in human patients. In 2006, Yamanaka of Kyoto University first demonstrated a novel approach for the preparation of induced pluripotent stem cells (iPSCs), which displayed similar pluripotency potential to embryonic stem cells (ESCs). Currently, iPSCs studies are permeating many sectors of disease research. Patient sample-derived iPSCs can be used to construct patient-specific disease models to elucidate the pathogenic mechanisms of disease development and to test new therapeutic strategies. Accordingly, the present review will focus on recent progress in iPSC research in the modeling of neurodegenerative disorders and in the development of novel therapeutic options.
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Dissertations / Theses on the topic "Neurodegenerative disease modeling"

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Lorenzo, Vivas Erica. "lnduced Pluripotent Stem cells disease modeling: approaching Gaucher and Tay Sachs." Doctoral thesis, Universitat de Barcelona, 2013. http://hdl.handle.net/10803/128928.

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IPSC are potent tools in the creation of disease models for both basic studies on the disease and testing of potential therapeutical drugs. In this context, it has been developed the derivation of iPSC from patient fibroblasts suffering from Gaucher Disease (GD) or Tay Sachs disease (TS). GD is a recessive autosomic disease which is characterized by the deficiency of the enzyme called glucocerebrosidase (GBA), which leads to the accumulation of its substrate glucosylceramide in macrophages and neurons. This disease has 3 forms of clinical presentation: type I, which is systemic; type II, the most severe with a neuronopathic acute presentation; type III, which is a combination of the former two, but without the severity of the type II. Tay Sachs is an autosomic recessive disease which is characterized by the Hexosaminidase A (HexA) deficiency, which leads to GM2 accumulation on the lysosomes of neurons. Patients present neurodegeneration and severe impairment of the brain which ultimately leads to their death. In this project iPSC derived from GD and TS patient fibroblasts. Pluripotent state of the derived iPSC has been characterized. Later, iPSC have been differentiated to neurons in order to confirm the disease phenotype on the in vitro differentiated tissue. In GD the phenotype was corroborated by enzymatic assays and GBA detection by Western blot. A lower GBA activity on GD neurons compared to WT was found, consistent with the minor GBA levels in GD neurons detected in the western blot. In TS, derived neurons were analyzed by immunofluorescence for Lamp2 (lysosome marker), observing an increase in size and number on the TS neurons in contrast to WT. Also, TS neurons were analyzed by transmission electron microscopy, presenting membranous lamellar bodies in the cytosol of TS. Both iPSC diseases have been used as a platform for testing therapeutical drugs efficiency on the iPSC derived neurons.
Las iPS (células pluripotentes inducidas) se han revelado como potentes herramientas en la creación de modelos de enfermedades humanas para su estudio y el testeo de potenciales drogas. En este marco hemos desarrollado un proyecto para derivar iPS de fibroblastos de pacientes de Gaucher y Tay Sachs, ambas enfermedades monogénicas recesivas. La enfermedad de Gaucher se caracteriza por la deficiencia de la glucocerebrosidasa (GBA), lo que conlleva la acumulación de su substrato, la glucosilceramida, en macrófagos y neuronas. Esta enfermedad tiene tres presentaciones I, que es sistémica; II, que es una forma neuronopática aguda, tiene efectos fatales ya que los pacientes rara vez sobreviven a los dos años de edad; y III, que es una mezcla de las dos anteriores, siendo neuronopática crónica, sin llegar a la severidad del tipo II. Tay Sachs es una enfermedad que se caracteriza por la deficiencia de la Hexosaminidasa A (HexA) lo que conlleva el almacenamiento en el lisosoma del gangliósido GM2. Los pacientes de esta enfermedad presentan daños neurológicos, provocando la muerte en la mayoría de los casos. En este proyecto se han desarrollado las iPS derivadas de fibroblastos de un paciente de Gaucher tipo II, y de otro de Tay Sachs. Las iPS resultantes de ambas enfermedades han sido caracterizadas para constatar su estado pluripotente y diferenciadas a neuronas para comprobar que presentan el fenotipo característico de las enfermedades. En el caso de Gaucher, mediante ensayos enzimáticos y detección de la GBA1 por western blot, detectando una menor actividad en las neuronas gaucher que en las WT, lo que es consecuente con la menor cantidad de GBA1 detectada. En el caso de Tay Sachs, las neuronas se han analizado mediante inmunohistoquímica, marcando Lamp2, típico de lisosomas y se ha observado un aumento de tamaño y cantidad respecto de las células WT diferenciadas en paralelo. También han sido analizadas por microscopía electrónica, presentando una acumulación de cuerpos laminares en los lisosomas y aumento de número y tamaño de éstos. Ambas enfermedades han sido utilizadas como modelos para probar compuestos en las neuronas derivadas de las iPS derivadas de fibroblastos del paciente y comprobar su eficacia.
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Toglia, Patrick. "Analyzing the effects of Ca2+ dynamics on mitochondrial function in health and disease." Scholar Commons, 2018. https://scholarcommons.usf.edu/etd/7652.

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Mitochondria plays a crucial role in cells by maintaining energy metabolism and directing cell death mechanisms by buffering calcium (Ca2+ )from cytosol. Therefore, the Ca2+ overload of mitochondria due to the upregulated cytosolic Ca2+ , observed in many neurological disorders is hypothesized to be a key pathway leading to mitochondrial dysfunction and cell death. In particular, Ca2+ homeostasis disruptions due to Alzheimer’ s disease (AD)-causing presenilins (PS1/PS2) and oligomeric forms of β-amyloid peptides Aβ commonly found in AD patients are presumed to cause detrimental effects on the mitochondria and its ability to function properly. We begin by showing that Familial Alzheimer’s disease (FAD)-causing PS mutants affect intracellular Ca2+ ([Ca2+]i) homeostasis by enhancing the gating of inositol 1,4,5-trisphosphate (IP3) receptor (IP3R) Ca2+ channels on the endoplasmic reticulum (ER), leading to exaggerated Ca2+ release into the cytoplasm. Using experimental IP3R-mediated Ca2+ release data in conjunction with a computational model of mitochondrial bioenergetics, we explore how the differences in mitochondrial Ca2+ uptake in control cells and cells expressing FAD-causing PS mutants affect key variables such as ATP, reactive oxygen species (ROS), NADH, and mitochondrial Ca2+ ([Ca2+ ]m). We find that as a result of exaggerated [Ca2+]i in FAD-causing mutant PS-expressing cells, the rate of oxygen consumption increases dramatically and overcomes the Ca2+ dependent enzymes that stimulate NADH production. This leads to decreased rates of proton pumping due to diminished membrane potential (Ψm) along with less ATP and enhanced ROS production. These results show that through Ca2+ signaling disruption, mutant PS leads to mitochondrial dysfunction and potentially cell death. Next, the model for the mitochondria is expanded to include the mitochondrial uniporter (MCU) that senses Ca2+ in the microdomain formed by the close proximity of mitochondria and ER. Ca2+ concentration in the microdomain ([Ca2+] mic) depends on the distance between the cluster of IP3R channels (r) on ER and mitochondria, the number of IP3R in the cluster (nIP3R), and open-probability (Po) of IP3R. Using the same experimental results for Ca2+ release though IP3R due to FAD-causing PS mutants, in conjunction with a computational model of mitochondrial bioenergetics, a data-driven Markov chain model for IP3R gating, and a model for the dynamics of the mitochondrial permeability transition pore (PTP), we explore the difference in mitochondrial Ca2+ uptake in cells expressing wild type (PS1-WT) and FAD-causing mutant (PS1-M146L) PS. We find that increased mitochondrial [Ca2+]m due to the gain-of-function enhancement of IP3R channels in the cell expressing PS1-M146L leads to the opening of PTP in high conductance state (PTPh), where the latency of opening is inversely correlated with r and proportional to nIP3R. Furthermore, we observe diminished inner mitochondrial Ψm, [NADH], [Ca2+]m, and [ATP] when PTP opens. Additionally, we explore how parameters such as the pH gradient, inorganic phosphate concentration, and the rate of the Na+/ Ca2+ -exchanger affect the latency of PTP to open in PTPh. Intracellular accumulation of oligomeric forms of Aβ are now believed to play a key role in the early phase of AD as their rise correlates well with the early symptoms of the disease. Extensive evidence points to impaired neuronal Ca2+ homeostasis as a direct consequence of the intracellular Aβ oligomers. To study the effect of intracellular Aβ on Ca2+ signaling and the resulting mitochondrial dysfunction, we employed data-driven modeling in conjunction with total internal reflection fluorescence (TIRF) microscopy (TIRFM). High resolution fluorescence TIRFM together with detailed computational modeling provides a powerful approach towards the understanding of a wide range of Ca2+ signals mediated by the IP3R. Achieving this requires a close agreement between Ca2+ signals from computational models and TIRFM experiments. However, we found that elementary Ca2+ release events, puffs, imaged through TIRFM do not show the rapid single-channel opening and closing during x and between puffs using data-driven single channel models. TIRFM also shows a rapid equilibration of 10 ms after a channel opens or closes which is not achievable in simulation using standard Ca2+ diffusion coefficients and reaction rates between indicator dye and Ca2+. Using the widely used Ca2+ diffusion coefficients and reaction rates, our simulations show equilibration rates that are eight times slower than TIRFM imaging. We show that to get equilibrium rates consistent with observed values, the diffusion coefficients and reaction rates have to be significantly higher than the values reported in the literature. Once a close agreement between experiment and model is achieved, we use multiscale modeling in conjunction with patch-clamp electrophysiology of IP3R and fluorescence imaging of whole-cell Ca2+ response, induced by intracellular Aβ42 oligomers to show that Aβ42 inflicts cytotoxicity by impairing mitochondrial function. Driven by patch-clamp experiments, we first model the kinetics of IP3R, which is then extended to build a model for the whole-cell Ca2+ signals. The whole-cell model is then fitted to fluorescence signals to quantify the overall Ca2+ release from the ER by intracellular Aβ42 oligomers through G-protein-mediated stimulation of IP3 production. The estimated IP3 concentration as a function of intracellular Aβ42 content together with the whole-cell model allows us to show that Aβ42 oligomers impair mitochondrial function through pathological Ca2+ uptake and the resulting reduced mitochondrial inner membrane potential, leading to an overall lower ATP and increased production of reactive oxygen species and [H2O2]. We further show that mitochondrial function can be restored by the addition of Ca2+ buffer EGTA, in accordance with the observed abrogation of Aβ42 cytotoxicity by EGTA in our live cells experiments. Finally, our modeling study was extended to other pathological phenomena such as epileptic seizures and spreading depolarizations (SD) and their effects on mitochondria by incorporating conservation of particles and charge, and accounting for the energy required to restore ionic gradients to the neuron. By examining the dynamics as a function of potassium and oxygen we can account for a wide range of neuronal hyperactivity from seizures, normoxic SD, and hypoxic SD (HSD) in the model. Together with a detailed model of mitochondria xi and Ca2+ -release through the ER, we determine mitochondrial dysfunction and potential recovery mechanisms from HSD. Our results demonstrate that HSD causes detrimental mitochondrial dysfunction that can only be recovered by restoration of oxygen. Once oxygen is replenished to the neuron, organic phosphate and pH gradients along the mitochondria determine how rapid the neuron recovers from HSD.
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Laranjeira, Simão. "Modelling the progression of neurodegenerative diseases." Thesis, University of Oxford, 2017. https://ora.ox.ac.uk/objects/uuid:ebb621d0-e4e6-405e-9e54-ba385c3ebd0a.

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Neurodegenerative disease is an umbrella term for pathologies that primarily damage neurons. As their incidence increases with age it is becoming of a greater concern for the west, due to its aging population. Due to their chronic nature and the difficulty to create reliable and reproducible animal models of these diseases their pathophysiologies are still poorly understood. For all these reasons, a mathematical modelling approach is suggested. The methodology of the work here consisted of identifying the state of the art models that describe the healthy behaviour of cells (e.g. metabolism and ionic regulation) and adapting them for pathological environments. With these models hypotheses provided by clinicians and pathologists were tested. The work focuses on developing models of mechanisms common to neurodegenerative diseases, which include: glutamate excitotoxicity, aquaporin water kinetics, inflammatory complement lysis and acute inflammation. Glutamate excitotoxicity was modelled by creating a compartmental model of glutamate exchange between neurons and astrocytes. This model was the first model of glutamate kinetics validated in an ischaemic stroke context. The aquaporin water kinetics and complement lysis models were developed in the context of the autoimmune disease Neuromyelitis Optica. Through this project a hypothesised trigger for the pathology was confirmed. Additionally, the first model of astrocytic cytotoxic oedema due to complement lysis was developed. Finally, a preventative drug for complement lysis was simulated. Acute inflammation was explored in the context of understanding the potential of chemerin as a pro-resolving cytokine. To that effect, a model of acute inflammation was developed where pro-resolving mechanisms were included. This model was the first to attempt model the effects of an intervention in inflammation. The results indicated that there is a maximum inhibitory effect of chemerin on inflammation. Additionally, two preventive avenues for chronic inflammation were found. With this work, the first attempts of capturing relevant mechanisms of neurodegenerative diseases were presented. These models can now be further developed and adapted to other pathological environments.
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Cemal, Cemal Kubilay. "Modelling Machado-Joseph disease by YAC transgenesis." Thesis, Imperial College London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367616.

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Traini, Mathew Biotechnology &amp Biomolecular Sciences Faculty of Science UNSW. "Modelling aspects of neurodegeneration in Saccharomyces cerevisiae." Publisher:University of New South Wales. Biotechnology & Biomolecular Sciences, 2009. http://handle.unsw.edu.au/1959.4/43383.

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The neurodegenerative disorders Alzheimer??s Disease (AD) and Parkinson??s Disease (PD) are characterised by the accumulation of misfolded amyloid beta 1-42 peptide (Aβ1-42) or α-synuclein, respectively. In both cases, there is extensive evidence to support a central role for these aggregation-prone molecules in the progression of disease pathology. However, the precise mechanisms through which Aβ1-42 and α-synuclein contribute to neurodegeneration remain unclear. Organismal, cellular and in vitro models are under development to allow elucidation of these mechanisms. A cellular system for the study of intracellular Aβ1-42 misfolding and localisation was developed, based on expression of an Aβ1-42-GFP fusion protein in the model eukaryote Saccharomyces cerevisiae. This system relies on the known inverse relationship between GFP fluorescence, and the propensity to misfold of an N-terminal fusion domain. To discover cellular processes that may affect the misfolding and localisation of intracellular Aβ1-42, the Aβ1-42-GFP reporter was transformed into the S. cerevisiae genome deletion mutant collection and screened for fluorescence. 94 deletion mutants exhibited increased Aβ1-42-GFP fluorescence, indicative of altered Aβ1-42 misfolding. These mutants were involved in a number of cellular processes with suspected relationships to AD, including the tricarboxylic acid cycle, chromatin remodelling and phospholipid metabolism. Detailed examination of mutants involved in phosphatidylcholine synthesis revealed the potential for phospholipid composition to influence the intracellular aggregation and localisation of Aβ1-42. In addition, an existing S. cerevisiae model of α-synuclein pathobiology was extended to study the effects of compounds that have been hypothesized to be environmental risk factors leading to increased risk of developing PD. Exposure of cells to aluminium, dieldrin and compounds generating reactive oxygen species enhanced the toxicity of α- synuclein expression, supporting suggested roles for these agents in the onset and development of PD. Expression of α-synuclein-GFP in phosphatidylcholine synthesis mutants identified in the Aβ1-42-GFP fluorescence screen resulted in dramatic alteration of α-synuclein localisation, indicating a common involvement of phospholipid metabolism and composition in modulating the behaviours of these two aggregation-prone proteins.
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BORDONI, MATTEO. "Development of innovative three dimensional cell culture for modeling neurodegenerative diseases." Doctoral thesis, Università degli studi di Pavia, 2019. http://hdl.handle.net/11571/1248528.

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BORDONI, MATTEO. "Development of innovative three dimensional cell culture for modeling neurodegenerative diseases." Doctoral thesis, Università degli studi di Pavia, 2019. http://hdl.handle.net/11571/1248548.

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BORDONI, MATTEO. "Development of innovative three dimensional cell culture for modeling neurodegenerative diseases." Doctoral thesis, Università degli studi di Pavia, 2019. http://hdl.handle.net/11571/1263909.

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BORDONI, MATTEO. "Development of innovative three dimensional cell culture for modeling neurodegenerative diseases." Doctoral thesis, Università degli studi di Pavia, 2019. http://hdl.handle.net/11571/1264029.

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BORDONI, MATTEO. "Development of innovative three dimensional cell culture for modeling neurodegenerative diseases." Doctoral thesis, Università degli studi di Pavia, 2019. http://hdl.handle.net/11571/1263888.

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Books on the topic "Neurodegenerative disease modeling"

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Staats, Kim A., Kyle David Fink, and Dustin R. Wakeman, eds. Stem Cells in Neurodegeneration: Disease Modeling and Therapeutics. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88971-182-6.

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van der Burg, Jorien M. M., N. Ahmad Aziz, and Maria Björkqvist. Peripheral Pathology. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199929146.003.0014.

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Clinicians and researchers have previously focused on the neurologic and psychiatric aspects of Huntington’s disease (HD). However, it is becoming evident that many neurodegenerative disorders are also complicated by pathology in tissues outside the brain. Although many clinical features of HD can be ascribed to neuronal loss and dysfunction, there is accumulating evidence indicating a role for the pathology of non-neuronal tissues in the disease process. Mutant huntingtin is expressed throughout the body and may induce pathology in parallel in both the brain and other organs. Insights into peripheral pathology in HD have the potential of improving knowledge of key pathogenic mechanisms. This chapter describes peripheral manifestations of HD, including weight loss, muscle wasting, and cardiac dysfunction, and discusses how these might constitute targets for drug treatment as well as offering disease modeling systems and potential sources of biomarkers.
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Logie, Robert, Valerie Camos, and Nelson Cowan, eds. Working Memory. Oxford University Press, 2020. http://dx.doi.org/10.1093/oso/9780198842286.001.0001.

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Working memory refers to how we keep track of what we are doing moment to moment throughout our waking lives. It allows us to remember what we have just done, focus on what we are doing now, to solve problems, be creative, think about what we will be doing in the next few seconds, and continually to update in our mind changes around us throughout the day. This book brings together in one volume, state-of-the-science chapters written by some of the most productive and well-known working memory researchers worldwide. Chapters cover leading-edge research on working memory, using behavioural experimental techniques, neuroimaging, computational modelling, development across the healthy human lifespan, and studies of neurodegenerative disease and focal brain damage. A unique feature of the book is that each chapter starts with answers to a set of common questions for all authors. This allows readers very rapidly to compare key differences in theoretical assumptions and approaches to working memory across chapters, and to understand the theoretical context before going on to read each chapter in detail. All authors also have been asked to consider evidence that is not consistent with their theoretical assumptions. It is very common for authors to ignore contradictory evidence. This approach has led to new interpretations and new hypotheses for future research to greatly enhance our understanding of this crucial human ability.
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Book chapters on the topic "Neurodegenerative disease modeling"

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Avramouli, Antigoni, and Panagiotis Vlamos. "Neurodegenerative Disease Modeling: An Introduction." In Handbook of Computational Neurodegeneration, 3–10. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-319-75922-7_68.

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Avramouli, Antigoni, and Panagiotis M. Vlamos. "Neurodegenerative Disease Modeling: An Introduction." In Handbook of Computational Neurodegeneration, 1–8. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-319-75479-6_68-1.

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Ameen, Ganna, and Basant Osama. "Modeling Neural Circuits in Parkinson’s Disease." In Handbook of Neurodegenerative Disorders, 1–37. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-19-3949-5_46-1.

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Komen, Johannes C., and David R. Thorburn. "Modeling Mitochondrial Dysfunction in Neurodegenerative Disease." In Mitochondrial Dysfunction in Neurodegenerative Disorders, 193–212. London: Springer London, 2011. http://dx.doi.org/10.1007/978-0-85729-701-3_12.

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Oxtoby, Neil P. "Data-Driven Disease Progression Modeling." In Machine Learning for Brain Disorders, 511–32. New York, NY: Springer US, 2012. http://dx.doi.org/10.1007/978-1-0716-3195-9_17.

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AbstractIntense debate in the neurology community before 2010 culminated in hypothetical models of Alzheimer’s disease progression: a pathophysiological cascade of biomarkers, each dynamic for only a segment of the full disease timeline. Inspired by this, data-driven disease progression modeling emerged from the computer science community with the aim to reconstruct neurodegenerative disease timelines using data from large cohorts of patients, healthy controls, and prodromal/at-risk individuals. This chapter describes selected highlights from the field, with a focus on utility for understanding and forecasting of disease progression.
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Fischer, D. Luke, Sara E. Gombash, Christopher J. Kemp, Fredric P. Manfredsson, Nicole K. Polinski, Megan F. Duffy, and Caryl E. Sortwell. "Viral Vector-Based Modeling of Neurodegenerative Disorders: Parkinson’s Disease." In Gene Therapy for Neurological Disorders, 367–82. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3271-9_26.

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Young, Deborah. "Gene Therapy-Based Modeling of Neurodegenerative Disorders: Huntington’s Disease." In Gene Therapy for Neurological Disorders, 383–95. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3271-9_27.

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Lavin, Alexander. "Neuro-Symbolic Neurodegenerative Disease Modeling as Probabilistic Programmed Deep Kernels." In AI for Disease Surveillance and Pandemic Intelligence, 49–64. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-93080-6_5.

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Chen, Chih-Wei, Shang-Yu Wu, and Geng-Ming Hu. "Single Differentiated Neurons from Pluripotent Embryonic Stem Cells: Motor Protein Modeling and Neurodegenerative Disease." In Series in BioEngineering, 383–414. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-49118-8_15.

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Laird, Angela S., and Wim Robberecht. "Modeling Neurodegenerative Diseases in Zebrafish Embryos." In Methods in Molecular Biology, 167–84. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-328-8_11.

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Conference papers on the topic "Neurodegenerative disease modeling"

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M, M. Abdel-Aleim, Mohamed Hassan, and Fathy Abo Sree Mohamed. "Detecting Selected Neurodegenerative Diseases Through Microwave Technology: Modeling and Identifying Different Stages of Alzheimer's Disease." In 2024 6th International Youth Conference on Radio Electronics, Electrical and Power Engineering (REEPE). IEEE, 2024. http://dx.doi.org/10.1109/reepe60449.2024.10479753.

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Hamdeni, Tasnime, Soufiane Gasmi, Mounir Sayadi, and Jean-Marc Ginoux. "Statistical modeling for the prediction of survival rate in a neurodegenerative disease." In 2022 5th International Conference on Advanced Systems and Emergent Technologies (IC_ASET). IEEE, 2022. http://dx.doi.org/10.1109/ic_aset53395.2022.9765831.

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Pitta, Marina Galdino da Rocha, Jordy Silva de Carvalho, Luzilene Pereira de Lima, and Ivan da Rocha Pitta. "iPSC therapies applied to rehabilitation in parkinson’s disease." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.022.

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Background: Parkinson’s disease (PD) is a neurological disorder that affects movement, mainly due to damage and degeneration of the nigrostriatal dopaminergic pathway. The diagnosis is made through a clinical neurological analysis where motor characteristics are considered. There is still no cure, and treatment strategies are focused on symptoms control. Cell replacement therapies emerge as an alternative. Objective: This review focused on current techniques of induced pluripotent stem cells (iPSCs). Methods: The search terms used were: “Parkinson’s Disease”, “Stem cells” and “iPSC”. Open articles written in English, from 2016-21 were selected in the Pubmed database, 10 publications were identified. Results: With the modernization of iPSC, it was possible to reprogram pluripotent human somatic cells and generate dopaminergic neurons and individual-specific glial cells. To understand the molecular basis, cell and animal models of neurons and organelles are currently being employed. Organoids are derived from stem cells in a three-dimensional matrix, such as matrigel or hydrogels derived from animals. The neuronal models are: α-synuclein (SNCA), leucine-rich repeat kinase2 (LRRK2), PARK2, putative kinase1 induced by phosphatase and tensin homolog (PINK1), DJ-1. Both models offer opportunities to investigate pathogenic mechanisms of PD and test compounds on human neurons. Conclusions: Cell replacement therapy is promising and has great capacity for the treatment of neurodegenerative diseases. Studies using iPSC neuron and PD organoid modeling is highly valuable in elucidating relevants neuronal pathways and therapeutic targets, moreover providing important models for testing future therapies.
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Kuznetsov, Andrey V. "Modeling the Effect of Vesicle Traps on Mass Transfer and Traffic Jam Formation in Fast Axonal Transport." In 2010 14th International Heat Transfer Conference. ASMEDC, 2010. http://dx.doi.org/10.1115/ihtc14-22169.

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This paper simulates effects of structural changes in the microtubule (MT) system on mass transfer in an axon. Understanding this process is important for understanding the underlying reasons for many neurodegenerative diseases, such as Alzheimer’s disease. In particular, it is investigated how the degree of polar mismatching in an MT swirl affects organelle trap regions in the axon and inhibiting transport of organelles down the axon. The model is based on modified Smith-Simmons equations governing molecular-motor-assisted transport in neurons. It is established that the structure that develops as a result of a region with disoriented MTs (the MT swirl) consists of two organelle traps, the trap to the left of the swirl region accumulates plus-end oriented organelles and the trap to the right of this region accumulates minus-end oriented organelles. The presence of such a structure is shown to decrease the transport of organelles toward the synapse of the axon. Four cases with a different degree of polar mismatching in the swirl region are investigated; the results are compared with simulations for a healthy axon, in which case organelle traps are absent.
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Winston, Sam E., Riley C. Dehmer, and Timothy A. Doughty. "Parkinsons Disease: Tremor Suppression With Wearable Device." In ASME 2021 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2021. http://dx.doi.org/10.1115/imece2021-70910.

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Abstract Parkinson’s Disease (PD) is a neurodegenerative disorder that affects nearly a million people in the United States. Hand tremors are a well-known symptom associated with PD and result in anxiety, frustration, and malnutrition. While there is no cure, several approaches attempt to treat the symptoms. Many are invasive, including the use of pharmaceuticals and surgery [1]. Noninvasive technologies are often cumbersome and do not address the conspicuous nature experiencing tremors in public. This study is motivated by design criteria established from previous research [2], with a goal of an affordable, purely mechanical solution. In both cases, human subject testing echoed lab tests in effective tremor reduction. The extension to a wearable device gives the user the ability to hold or handle any object, or no object, with a significant reduction in tremor. Two separate wearable devices were tested for effectiveness while the simulated user ‘held’ two different objects to simulate different applications. Biomechanical modeling of the human hand informed the development of an adjustable mechanical hand-tremor system for testing. Models of the devices and the hand-device interface were used to simulate the dynamic response of the coupled systems. Each device was secured to the mechanical hand-tremor system and harmonic stimulus and response data was collected over the range of typical tremor frequencies. The results demonstrate the versatility of both designs for reducing the oscillations associated with tremors. The Ratio of Reduction (RoR) was defined to compare the tremor amplitude of the hand-tremor system with and without the device. Both designs were considered effective for each object with a max RoR of 28.09 for Device A and a max RoR of 99.32 for Device B.
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Yildiz, Ahmet, Timothy Minicozzi, Franklin King, Fumirato Masaki, Garth Rees Cosgrove, Walid Ibn Essayed, and Nobuhiko Hata. "Skull-mounted guidance device for intraoperative CT-guided DBS of neurodegenerative diseases." In Image-Guided Procedures, Robotic Interventions, and Modeling, edited by Cristian A. Linte and Jeffrey H. Siewerdsen. SPIE, 2022. http://dx.doi.org/10.1117/12.2611426.

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Elden, Rana Hossam, Walid Al-Atabany, and Vidan Fathi Ghoneim. "Gait Variability Analysis in Neurodegenerative Diseases Using Nonlinear Dynamical Modelling." In 2018 9th Cairo International Biomedical Engineering Conference (CIBEC). IEEE, 2018. http://dx.doi.org/10.1109/cibec.2018.8641835.

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Madhushree, B. A., Nandyala D. Gangadhar, and K. S. Prafulla Kumari. "Modelling and Mining Brain Network Data for Diagnosis of Neurodegenerative Diseases." In 2020 IEEE International Conference on Electronics, Computing and Communication Technologies (CONECCT). IEEE, 2020. http://dx.doi.org/10.1109/conecct50063.2020.9198380.

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Schaffer, W. M., and T. V. Bronnikova. "Modeling Peroxidase-Oxidase Interactions." In ASME 2011 Dynamic Systems and Control Conference and Bath/ASME Symposium on Fluid Power and Motion Control. ASMEDC, 2011. http://dx.doi.org/10.1115/dscc2011-5946.

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Reactive oxygen species (ROS) and peroxidase-oxidase (PO) reactions are Janus-faced contributors to cellular metabolism. At low concentrations, reactive oxygen species serve as signaling molecules; at high concentrations, as destroyers of proteins, lipids and DNA. Correspondingly, PO reactions are both sources and consumers of ROS. In the present paper, we study a well-tested model of the PO reaction based on horseradish peroxidase chemistry. Our principal predictions are these: 1. Under hypoxia, the PO reaction can emit pulses of hydrogen peroxide at apparently arbitrarily long intervals. 2. For a wide range of input rates, continuing infusions of ROS are transduced into bounded dynamics. 3. The response to ROS input is hysteretic. 4. With sufficient input, regulatory capacity is exceeded and hydrogen peroxide, but not superoxide, accumulates. These results are discussed with regard to the episodic nature of neurodevelopmental and neurodegenerative diseases that have been linked to oxidative stress and to downstream interactions that may result in positive feedback and pathology of increasing severity.
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