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341 results for “Neurodegeneration”
The Yin and Yang of RNA in neurodegeneration | Talk - I PhasAGE International Conference
<p>The <strong>I PhasAGE international conference</strong> brought together members of the PhasAGE consortium as well as outstanding international speakers showcasing high impact achievements in the field of liquid-liquid phase separation in aging and late-onset diseases.</p> <p>For details on conference program please see: https://phasage.eu/phasage-conference-1/ </p>
Aggregating gut: on the link between neurodegeneration and bacterial functional amyloids - Datasets
<p>This repository contains data from work "Aggregating gut: on the link between neurodegeneration and bacterial functional amyloids"<br><br></p> <p><a href="https://zenodo.org/api/records/14016809/draft/files/BFA.fasta/content" target="_blank" rel="noopener noreferrer">BFA.fasta</a> - fasta file containing sequences of bacterial functional amyloids used as a query for identification of novel bacterial functional amyloids in UHGP dataset</p> <p><a href="https://zenodo.org/api/records/14016809/draft/files/UHGPAmyloids.fasta/content" target="_blank" rel="noopener noreferrer">UHGPAmyloids.fasta </a>- fasta file containing sequences of amyloids identified in UHGP dataset</p> <p><a href="https://zenodo.org/api/records/14016809/draft/files/UHGPAmyloids.csv/content" target="_blank" rel="noopener noreferrer">UHGPAmyloids.csv</a> - csv file containing information about amyloids identified in UHGP</p> <p>Columns:<br>query_id - Uniprot id of the protein from BFA<br>query_gene_name - gene name of the protein from BFA<br>target_id - UHGP id of the found homolog<br>ProbabilityAMYPred-FRL - score obtained for the target_id sequence according to AMYPred-FRL<br>Archcandy - Prediction of beta arch motif for identified amyloid<br>Genome - UHGP genome id of the target_id<br>Localization - predicted subcellular localization with BUSCA for target_id sequence<br>Lineage - full taxonomy of the target_id sequence (which bacteria produced this specific sequence) </p> <p><a href="https://zenodo.org/api/records/14016809/draft/files/PPIPositivePredictionsBetween_UHGPAmyloids_And_HPAIntestine_filtered.csv/content" target="_blank" rel="noopener noreferrer">PPIPositivePredictionsBetween_UHGPAmyloids_And_HPAIntestine_filtered.csv</a> - csv file contining inforamtions about predicted protein-protein interactions between UHGPAmyloids and human proteins expressed in guts</p> <p>Columns:<br>UHGPAmyloids_id - UHGPAmyloids id (same as target_id in UHGPAmyloids.csv)<br>hp_uniprot_name - Uniprot name of a human protein<br>negative and score - scores returned by ProteinPrompt softwawre for prediction of PPI<br>hp_uniprot_id - Uniprot id of a human protein<br>BFA_sp_uniprot_id - Uniprot id of a BFA source protein<br>BFA_sp_uniprot_name - gene name of a BFA source protein<br>UHGPAmyloids_localization - predicted subcellular localization with BUSCA for UHGPAmyloids_id sequence<br>UHGPAmyloids_lineage - full taxonomy of the UHGPAmyloids_id sequence (which bacteria produced this specific sequence) </p>
dataset related to article: " Cerebrospinal fluid neuropathological biomarkers in beta-propeller protein-associated neurodegeneration, with complicated parkinsonian phenotype"
<p>analysis sanger electropherograms in the patient's in .abi format and segregation in the family (mother; father and sister</p>
Data From: Global huntingtin knockout in adult mice leads to fatal neurodegeneration that spares the pancreas
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Biomarkers of neurodegeneration in isolated and antidepressant-related REM sleep behavior disorder.
<p>Dataset relative to the manuscript "Biomarkers of neurodegeneration in isolated and antidepressant-related REM sleep behavior disorder."</p>
Processed FDG-PET data from: A computational model of neurodegeneration in Alzheimer's disease
<p>Disruption of mental functions in Alzheimer's disease (AD) and related disorders is accompanied by selective degeneration of brain regions. These regions comprise large-scale ensembles of cells organized into systems for mental functioning, however the relationship between clinical symptoms of dementia, patterns of neurodegeneration, and functional systems is not clear. We developed a model of the association between dementia symptoms and degenerative brain anatomy using F18-fluorodeoxyglucose (FDG) PET and dimensionality reduction techniques patients with AD. This data and code package contains preprocessed FDG-PET images from 423 subjects across the Alzheimer's disease spectrum and the MATLAB code to produce eigenbrains from this data.</p>
The c-Abl inhibitor IkT-148009 therapeutically suppresses neurodegeneration in models of heritable and sporadic Parkinson's Disease
<p>Parkinson's Disease (PD) is the second most prevalent neurodegenerative disease of the central nervous system, with an estimated 5,000,000 cases worldwide. PD pathology is characterized by the accumulation of misfolded a-synuclein, which is thought to play a critical role in the etiopathogenesis of the disease. Animal models of PD suggest that activation of the Abelson Tyrosine Kinase, or c-Abl, plays an essential role in the initiation and progression of a-synuclein pathology and initiates processes leading to the degeneration of dopaminergic and non-dopaminergic neurons. Given the essential role of c-Abl in the disease, a proprietary c-Abl inhibitor library was developed to identify potent, orally bioavailable c-Abl inhibitors capable of crossing the blood-brain barrier based on pre-defined characteristics, leading to the discovery of IkT-148009. IkT-148009 is a selective, potent, brain-penetrant c-Abl inhibitor with a favorable toxicology profile that was analyzed for therapeutic potential in animal models of slowly progressive, a-synuclein-dependent disease. In models of both inherited and sporadic Parkinson's disease in the mouse, IkT-148009 suppressed c-Abl activation to baseline and substantially protected neurons from degeneration when administered therapeutically by once daily oral gavage beginning four weeks after disease initiation. Recovery of normal behavioral function in diseased mice occurred within 8 weeks of initiating treatment and occurred concomitantly with a substantial reduction of a-synuclein pathology in the brain. These disease-modifying outcomes in mice suggest IkT-148009 has the potential to be a disease-modifying therapy in human disease.</p>
Systemic inflammation accelerates neurodegeneration in a rat model of Parkinson's disease overexpressing human alpha synuclein
<p><span>Parkinson’s disease (PD) involves genetic and<span> </span>environmental risk factors. Increasing research efforts have been made to understand how they interact<span> </span>to<span> </span>impair<span> </span>homeostasis<span> </span>and<span> </span>elevate<span> </span>risk. Inflammation could be one unifying factor. In this study, <em>wild-type</em> (WT) and overexpressing human </span><span>α</span><span>-synuclein (<em>Snca</em><sup>+/+</sup>) rats <span>were intraperitoneally injected with a single dose of </span>lipopolysaccharide<span> </span>(LPS) or with saline (SAL). In these animals we assessed </span><span>the development of PD-like symptoms by immunohistology, high-dimensional flow cytometry, electrophysiology, and behavioral analyses. A single injection of LPS to both WT and <em>Snca<sup>+/+</sup> </em>rats triggered long-lasting increased activation of pro-inflammatory microglial markers, infiltrating monocytes and T-lymphocytes. However, only LPS <em>Snca</em><sup>+/+</sup> rats displayed dopaminergic neuronal loss in the <em>substantia<span> </span>nigra pars compacta<span> </span></em>(SNpc), associated with a reduction of evoked dopamine<span> release </span>in the striatum. No significant<span> </span>changes were observed in the behavioral domain. </span></p> <p><span> </span></p>
Microglia-mediated T cell Infiltration Drives Neurodegeneration in Tauopathy
<p>Extracellular amyloid-β (Aβ) deposition as neuritic plaques and intracellular accumulation of hyperphosphorylated, aggregated tau as neurofibrillary tangles (NFT) are two of the characteristic hallmarks in Alzheimer’s disease (AD). The regional progression of brain atrophy in AD highly correlates with tau accumulation but not amyloid deposition and the mechanisms of tau-mediated neurodegeneration remain elusive. Innate immune responses represent a common pathway for the initiation and progression of some neurodegenerative diseases. To date, little is known about the extent or role of the adaptive immune response in the presence of Aβ or tau pathology. We systematically compared the immunological milieus in the brain of mice with amyloid deposition or tau aggregation and neurodegeneration. We found that mice with tauopathy but not amyloid, developed a unique innate and adaptive immune response and that depletion of microglia or T-cells blocked tau-mediated neurodegeneration. T cells, especially cytotoxic T cells, were markedly increased in areas with tau pathology in mice with tauopathy and in the AD brain. T cell numbers correlated with the extent of neuronal loss, and dynamically transformed their cellular characteristics from activated to exhausted states along with unique TCR clonal expansion. Inhibition of IFN-γ and PD-1signaling both significantly ameliorated brain atrophy. Our results thus reveal a tauopathy and neurodegeneration-related immune hub involving activated microglia and T cell responses, which could serve as therapeutic targets for preventing neurodegeneration in AD and primary tauopathies.</p>
An unbiased, automated platform for scoring dopaminergic neurodegeneration in C. elegans
<p><em><span>Caenorhabditis elegans</span></em><span> (<em>C. elegans</em>) has served as a simple model organism to study dopaminergic neurodegeneration, as it enables quantitative analysis of cellular and sub-cellular morphologies in live animals. These isogenic nematodes have a rapid life cycle and transparent body, making high-throughput imaging and evaluation of fluorescently tagged neurons possible. However, the current state-of-the-art method for quantifying dopaminergic degeneration requires researchers to manually examine images and score dendrites into groups of varying levels of neurodegeneration severity, which is time-consuming, subject to bias, and limited in data sensitivity. We aim to overcome the pitfalls of manual neuron scoring by developing an automated, unbiased image processing algorithm to quantify dopaminergic neurodegeneration in <em>C. elegans</em>. The algorithm can be used on images acquired with different microscopy setups and only requires two inputs: a maximum projection image of the four cephalic neurons in the <em>C. elegans</em> head and the pixel size of the user's camera. We validate the platform by detecting and quantifying neurodegeneration in nematodes exposed to rotenone, cold shock, and 6-hydroxydopamine using 63x epifluorescence, 63x confocal, and 40x epifluorescence microscopy, respectively. Analysis of tubby mutant worms with altered fat storage showed that, contrary to our hypothesis, increased adiposity did not sensitize to stressor-induced neurodegeneration. We further verify the accuracy of</span><span> the</span><span> algorithm by comparing code-generated, categorical degeneration results with manually scored dendrites of the same experiments. The platform, which detects 19 different metrics of neurodegeneration, can provide comparative insight into how each exposure affects dopaminergic neurodegeneration patterns. </span></p>
Efficacy and Safety Study of Deferiprone in Patients With Pantothenate Kinase-associated Neurodegeneration (PKAN)
ClinicalTrials.gov study NCT01741532. IPD Sharing: Not stated. Countries: 4. Publications: 1.
An unbiased, automated platform for scoring dopaminergic neurodegeneration in C. elegans
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Processed FDG-PET data from: A computational model of neurodegeneration in Alzheimer’s disease
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Lesion evolution and neurodegeneration in RVCL-S, a monogenic microvasculopathy
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The c-Abl inhibitor IkT-148009 therapeutically suppresses neurodegeneration in models of heritable and sporadic Parkinson’s Disease
Open the record for dataset details and reuse information.
Comprehensive Assessment of Neurodegeneration and Dementia
ClinicalTrials.gov study NCT03402919. IPD Sharing: YES. Countries: 1. Publications: 1.
Mitochondrial Membrane Protein Neurodegeneration (MPAN)
ClinicalTrials.gov study NCT05678790. IPD Sharing: YES. Countries: 1. Publications: 2.
Biomarkers of Neurodegeneration and Neuroplasticity in Parkinson's Disease Patients Treated by Bilateral M1-iTBS
ClinicalTrials.gov study NCT06840145. IPD Sharing: YES. Countries: 1. Publications: 1.
Brain Iron Toxicity and Neurodegeneration - A 7T MRI Study
ClinicalTrials.gov study NCT04992975. IPD Sharing: NO. Countries: 1. Publications: 1.
Ferrochelating Treatment in Patients Affected by Neurodegeneration With Brain Iron Accumulation (NBIA)
ClinicalTrials.gov study NCT00907283. IPD Sharing: Not stated. Countries: 1. Publications: 2.
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.