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2,888 results for “Alzheimer's disease”
Summary statistics for "Exome sequencing identifies rare damaging variants in ATP8B4 and ABCA1 as risk factors for Alzheimer's Disease"
<p>These are the burden test results (summary statistics) for the publication:</p> <p>"Exome sequencing identifies rare damaging variants in ATP8B4 and ABCA1 as risk factors for Alzheimer’s Disease",</p> <p>Nature Genetics, 2022.</p> <p> </p> <p><em>Format: tab-separated-value.</em></p> <p><em>Fields:</em></p> <ul> <li><em>gene_stable_id: Ensembl gene id</em></li> <li><em>gene_name: standard gene name</em></li> <li><em>pvalue: burden test significance (likelihood ratio test, population structure correction based on 6 PCA components)</em></li> <li><em>cmac_all: sum of minor allele dosages across all contributing samples and variants</em></li> <li><em>group: variant group (LOF, LOF+REVEL>=75, LOF+REVEL>=50, LOF+REVEL>=25, see publication methods for further selection criteria).</em></li> <li><em>beta/se: beta/se of logistic ordinal regression (see publication methods). Positive = risk-increasing. Negative = risk-decreasing.</em></li> </ul> <p> </p>
Data for: Tang et al., Interpretable classification of Alzheimer's disease pathologies with a convolutional neural network pipeline. bioRxiv 2018.
<p>Datasets containing 63 whole slide images (WSIs) and their segmented 256x256 pixel tiles with approximately 80,000 tile-level amyloid-β pathology expert annotations.</p> <p><strong>Paper</strong>: "Interpretable classification of Alzheimer's disease pathologies with a convolutional neural network pipeline", bioRxiv 454793; DOI: <a href="https://doi.org/10.1101/454793">https://doi.org/10.1101/454793</a>.</p> <p><strong>Details:</strong> A total of 63 WSIs for 63 unique decedent cases spanning Alzheimer’s disease (AD) to non-AD and possessing a variety of CERAD scores. WSIs comprise three datasets as follows:</p> <ol> <li><em>Development (Phases I-II)</em>. 33 WSIs used for convolutional neural network (CNN) model development (29 training, 4 validation).</li> <li><em>Hold-out (Phase III)</em>. 10 WSIs selected by an expert neuropathologist as a held-out test set to assess the generalizability of the CNN model.</li> <li><em>CERAD-like hold-out</em>. 20 blinded WSIs collected solely for use in a CERAD-like scoring comparison study.</li> </ol> <p>Datasets 1 and 2 were color-normalized and segmented to 256x256 pixel image tiles for model training set (61,370 images), validation set (8,630 images), and hold-out test set (10,873 images). Dataset 3 was color-normalized but not segmented.</p> <p>Expert labels of plaques for Dataset 1 and 2 tiles are included in corresponding CSV files.</p> <p><strong>Slide source and preparation:</strong> All samples were retrieved from archives of the University of California, Davis Alzheimer’s Disease Center Brain Bank (<a href="https://www.ucdmc.ucdavis.edu/alzheimers/">https://www.ucdmc.ucdavis.edu/alzheimers/</a>). Archival samples analyzed in this study were 5 μm formalin fixed, paraffin embedded sections of the superior and middle temporal gyrus from human brain. The tissue had been previously stained with an amyloid-β antibody (4G8, recognizing residues 17-24, BioLegend, formerly Covance) that were first pretreated with formic acid to rid samples of endogenous protein. All slides were digitized using an Aperio AT2 up to 40x magnification.</p> <p><strong>Code:</strong> Please visit <a href="https://github.com/keiserlab/plaquebox-paper">https://github.com/keiserlab/plaquebox-paper</a></p> <p> </p>
Atrophy Pattern Maps of Alzheimer's Disease, Mild Cognitive Impairment, Parkinson's Disease, and Frontotemporal Dementia
<p>The files contain voxel-wise t-statistics maps contrasting deformation based morphometry (DBM) measurements of Alzheimer's disease (AD), Parkinson's disease (PD), mild cognitive impairment (MCI), and fronto-temporal dementia (FTD) patients against matched normal controls.</p> <p>AD and MCI maps are based on ADNI data, available at:</p> <p>PD map is based on PPMI data, available at:</p> <p>FTD map is based on NIFD data, available at:</p> <p>For more information regarding the participants and method details, see:</p> <p>Dadar, Mahsa, et al. "White matter hyperintensities are associated with grey matter atrophy and cognitive decline in Alzheimer's disease and frontotemporal dementia." <em>Neurobiology of aging</em> 111 (2022): 54-63.</p>
Integrative in situ mapping of single-cell transcriptional states and tissue histopathology in an Alzheimer disease model
<p>Amyloid-β plaques and neurofibrillary tau tangles are the neuropathologic hallmarks of Alzheimer’s disease (AD), but the spatiotemporal cellular responses and molecular mechanisms underlying AD pathophysiology remain poorly understood. Here we introduce STARmap PLUS to simultaneously map single-cell transcriptional states and disease marker proteins in brain tissues of AD mouse models at a voxel size of 95 95 350 nm. This high-resolution spatial transcriptomics map revealed a core-shell structure where disease-associated microglia (DAM) closely contact amyloid-β plaques, whereas disease-associated astrocyte-like cells (DAA-like) and oligodendrocyte precursor cells (OPC) are enriched in the outer shells surrounding the plaque-DAM complex. Hyperphosphorylated tau emerged mainly in excitatory neurons in the CA1 region accompanied by infiltration of oligodendrocyte subtypes into the axon bundles of hippocampal alveus. The integrative STARmap PLUS method bridges single-cell gene expression profiles with tissue histopathology at subcellular resolution, providing an unprecedented roadmap to pinpoint the molecular and cellular mechanisms of AD pathology and neurodegeneration.</p>
Biochemical Characterization of Mouse Retina of an Alzheimer's Disease Model by Raman Spectroscopy
<p>Raman raw data for the paper "Biochemical Characterization of Mouse Retina of an Alzheimer’s Disease Model by Raman Spectroscopy"</p> <ul> <li>two datasets of Raman images from cross-sectional and en face mouse retinas without processing</li> </ul>
Resting-State High-Density EEG using EGI GES 300 with 256 Channels of Healthy Elders, People with Subjective and Mild Cognitive Impairment and Alzheimer's Disease
<p>This repository contains Matlab files including 4 samples of resting-state EEG recording for Alzheimer's Disease (AD), Mild Cognitive Impairment (MCI), Subjective Cognitive Decline (SCD), and Healthy Controls (HC) using the HD-EEG EGI GES 300.</p> <p><strong>[AD: i108, MCI: i100, SCD: i090, HC: s055]</strong></p> <p> </p> <p><strong>Participants & Settings</strong></p> <p>In total 230 participants have been recruited from the memory and dementia clinic of the Greek Association of Alzheimer’s Disease and Related Disorders (GAADRD) and the 1st Department of Neurology, U.H. AHEPA, Aristotle University of Thessaloniki, Greece.</p> <p>The full dataset includes:</p> <p><strong>Healthy Controls Elders (60+ years old)</strong>: 33 participants</p> <p><strong>Subjective Cognitive Decline:</strong> 34 participants</p> <p><strong>Mild Cognitive Impairment</strong>: 79 participants</p> <p><strong>Alzheimer's Disease</strong>: 48 participants</p> <p><strong>Healthy Young (25-40 years old):</strong> 36 participants</p> <p>The study was carried out in accordance with the Declaration of Helsinki and received approval by the Scientific and Ethics Committee of GAADRD (No56_27/11/2016), and written informed consent was obtained from all participants prior to their participation in the study. The diagnosis of AD was conducted by a neuropsychiatrist according to their medical history, neuropsychological performance, structural magnetic resonance imaging (MRI), and clinical and neurological examinations.</p> <p>Participants with AD fulfilled the National Institute of Neurological and Communication Disorders and Stroke/Alzheimer’s Disease and Related Disorders Association (NINCDS-ADRDA) criteria for probable AD, as well as the Diagnostic and Statistical Manual of Mental Disorders (DSM-V) criteria for dementia of Alzheimer’s type (American Psychological Association, 1994). On the other hand, the MCI participants fulfilled the Petersen criteria, while the SCD group met International Working Group-2 guidelines and the recent National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease (NI-AA), as well as the SCD-I Working Group instructions. </p> <p><strong>Resting-State EEG Recording</strong></p> <p>Fifteen-minute resting EEG activity was recorded for all the participants. For the whole duration of the resting state EEG recording, participants were advised to keep themselves relaxed as much as possible, close their eyes and open them after the researcher’s demand, sit still, minimize blinking or mouth movements and let their mind wander. The experimental procedure was monitored by a research assistant aiming to identify cases of horizontal eye movements, continued blinking, or excessive movement by visually inspecting the EEG traces during the experiment. More specifically, an EEG was registered for both resting conditions (eyes open, EO and eyes closed, EC) for at least 2–3 min for each period.</p> <p><strong>EEG Data Acquisition</strong></p> <p>The EEG data were collected by using the EGI 300 Geodesic EEG system (GES 300, CERTH-ITI, Thessaloniki, Greece) with a 256-channel HydroCel Geodesic Sensor Net (HCGSN) and a sampling rate of 250 Hz (EGI Eugene, OR). Moreover, the researcher placed the electrodes in accordance with the 256 HCGSN adult 1.0 montage system, while the signals were recorded relative to a vertex reference electrode (Cz), with AFz as the ground electrode with the electrodes’ impedance below 50 kΩ throughout the experimental procedure, as recommended for the high-input impedance amplifier. In detail, the HD-EEG data were analyzed offline in order to detect any artifact, as well as to conduct pre-processing (filtering, segmentation, bad channel replacement) using Net Station 4.3 software (EGI). HD-EEG data were initially filtered with a 5th-order bandpass Butterworth IIR filter of 0.3–30 Hz. Once the segmentation was completed, the detection of artifacts was performed by using the Net Station artifact detection tool for the automatic detection of excessive eye blinking and movement. Afterward, the signals were baseline corrected using 200 msec before the start of the experiment period and average re-referenced to transform them into reference-independent values.</p> <p> </p> <p><strong>Full Dataset Access</strong></p> <p>More information about the sample dataset and access to the full dataset can be available after request via e-mail:</p> <p><strong>Ioulietta Lazarou</strong> BSc, MSc, PhD candidate</p> <p>Neuropsychologist - Clinical Research Associate </p> <p>Centre for Research and Technology Hellas (CERTH), Information Technologies Institute (ITI)</p> <p>6th km Charilaou-Thermi Road, P.O. Box 60361, 57001 Thermi-Thessaloniki, Greece</p> <p>E-mail: <a href="mailto:iouliettalaz@iti.gr">iouliettalaz@iti.gr</a></p>
Data for Altered Glia-Neuron Communication in Alzheimer's Disease Affects WNT, p53, and NFkB Signaling Determined by snRNA-seq
<p><strong>data.tar.gz contains all files from the data directory associated with the 230313_TS_CCCinHumanAD GitHub project and includes the following:</strong></p><ul><li><strong>CellRangerCounts/</strong><ul><li><strong>GSE157827/</strong><ul><li><strong>post_soupX/ : </strong>contains 21 directories for 21 samples, which each contain 3 files obtained from ambient RNA removal with soupX. Below is a representative example, but this repo contains 1 directory per sample:<ul><li><strong>SAMN16100290_S01_AD/</strong><ul><li><strong>barcodes.tsv</strong></li><li><strong>genes.tsv</strong></li><li><strong>matrix.mtx</strong></li></ul></li></ul></li><li><strong>pre_soupX/ : </strong>contains 21 directories for 21 samples, which each contain 2 files obtained from Cell Ranger after aligning fastq files to the reference genome. Below is a representative example, but this repo contains 1 directory per sample:<ul><li><strong>SAMN16100290_S01_AD/</strong><ul><li><strong>filtered_feature_ bc_matrix.h5</strong></li><li><strong>Raw_feature_bc_matrix.h5</strong></li></ul></li></ul></li></ul></li><li><strong>GSE174367/ : </strong>contains 19 directories for 19 samples, which contain 3 files each from Cell Ranger alignment of fastq files to the reference genome. Below is a representative example, but this repo contains 1 directory per sample:<ul><li><strong>SAMN19128610_S1_CTRL/</strong><ul><li><strong>barcodes.tsv</strong></li><li><strong>genes.tsv</strong></li><li><strong>Matrix.mtx</strong></li></ul></li></ul></li></ul></li><li><strong>ccc/</strong><ul><li><strong>nichenet_grn/</strong><ul><li><strong>gr_network_human_21122021.rds : </strong>accessed in October 2023, gene regulation network – gene regulatory information from MultiNicheNet</li><li><strong>ligand_tf_matrix_nsga2r_final.rds: </strong>accessed in October 2023, ligand tf matrix for signaling path determination from MultiNicheNet</li><li><strong>signaling_network_human_21122021.rds : </strong>accessed in October 2023, signaling network – protein-protein interaction information from MultiNicheNet</li><li><strong>weighted_networks_nsga2r_final.rds : </strong>accessed in October 2023, networks weighted by literature evidence from MultiNicheNet</li></ul></li><li><strong>nichenet_prior/</strong><ul><li><strong>ligand_target_matrix.rds : </strong>accessed in April 2023, ligand to target matrix from NicheNet</li><li><strong>lr_network.rds : </strong>accessed in April 2023, ligand-receptor matrix from NicheNet</li></ul></li><li><strong>nichenet_v2_prior/</strong><ul><li><strong>ligand_target_matrix_nsga2r_final.rds : </strong>accessed in June 2023, ligand to target matrix from MultiNicheNet used to predict target genes.</li><li><strong>lr_network_human_21122021.rds : </strong>accessed in June 2023, ligand-receptor matrix from MultiNicheNet used to predict ligand-receptor pairs.</li></ul></li><li><strong>geo_multinichenet_output.rds </strong>: MultiNicheNet output for Morabito et al., 2021 data</li><li><strong>geo_signaling_igraph_objects.rds </strong>: list of igraph objects for 17 overlapping LRTs and their signaling mediators in the Morabito et al., 2021 dataset. </li><li><strong>gse_multinichenet_output.rds</strong> : MultiNicheNet output for Lau et al., 2020 data</li><li><strong>gse_signaling_igraph_objects.rds</strong> : list of igraph objects for 17 overlapping LRTs and their signaling mediators in the Lau et al., 2020 dataset </li></ul></li><li><strong>seurat_preprocessing/</strong><ul><li><strong>geo_filtered_seurat.rds : </strong>merged and filtered seurat object of Morabito et al., 2021 data</li><li><strong>geo_integrated_seurat.rds :</strong> seurat object integrated using harmony of Morabito et al., 2021 data</li><li><strong>geo_clustered_seurat.rds : </strong>clustered seurat object of Morabito et al., 2021 data</li><li><strong>geo_processed_seurat.rds : </strong>processed seurat object with final cell type assignments at specified resolution of Morabito et al., 2021 data</li><li><strong>gse_filtered_seurat.rds : </strong>merged and filtered seurat object of Lau et al., 2020 data</li><li><strong>gse_integrated_seurat.rds : </strong>seurat object integrated using harmony of Lau et al., 2020 data</li><li><strong>gse_clustered_seurat.rds :</strong> clustered seurat object of Lau et al., 2020 data</li><li><strong>gse_processed_seurat.rds : </strong>processed seurat object with final cell type assignments at specified resolution of Lau et al., 2020 data </li></ul></li></ul>
Tabular and image data of article "Morphing cholinesterase inhibitor amiridine into multipotent drugs for the treatment of Alzheimer's disease"
<p>The search for novel drugs to address the medical needs of Alzheimer’s disease (AD) is an ongoing process relying on the discovery of disease-modifying agents. Given the complexity of the disease, such an aim can be pursued by developing so-called multi-target directed ligands (MTDLs) that will impact the disease pathophysiology more<br>comprehensively. Herewith, we contemplated the therapeutic efficacy of an amiridine drug acting as a cholinesterase inhibitor by converting it into a novel class of novel MTDLs. Applying the linking approach, we have paired amiridine as a core building block with memantine/adamantylamine, trolox, and substituted benzothiazole moieties to generate novel MTDLs endowed with additional properties like N-methyl-D-aspartate (NMDA) receptor affinity, antioxidant capacity, and anti-amyloid properties, respectively. The top-ranked amiridine-based compound 5d was also inspected by in silico to reveal the butyrylcholinesterase binding differences with its close structural analogue 5b. Our study provides insight into the discovery of novel amiridinebased drugs by broadening their target-engaged profile from cholinesterase inhibitors towards MTDLs with potential implications in AD therapy.</p> <p><strong>Table 1. </strong>hBChE inhibitory activities of 5c-d, 7c and 7 g and reference compounds (amiridine hydrochloride and THA); their cytotoxicity profile on SH-SY5Y cell line, and predictions of BBB penetration.</p> <p>T<strong>able 2</strong>. Relative inhibitions (RIs) of 5c-d and 7 m and reference compound memantine at recombinant human GluN1/GluN2B NMDA receptor expressed in HEK293 cells.</p> <p><strong>Fig_1</strong>. Chemical structures of rivastigmine, galantamine, and tacrine as representatives of cholinesterase inhibitors. Approaches to novel drugs for AD treatment on the selected candidates are displayed.</p> <p><strong>Fig_2</strong>. Examples of previously published amiridine-based derivatives and design strategy applied in the current study below, using various pharmacophores.</p> <p><strong>Fig_3</strong>. Top scored docking pose of 5b (A) and 5d (B) highlighting the key findings responsible for compound activity/inactivity. For the sake of clarity, superimposed ligands are aligned in the Fig. C with respect to key amino acid residue W82 to demonstrate the binding difference. Compounds 5b and 5d are colored in salmon and yellow, respectively. Essential amino acid residues responsible for ligand anchoring are rendered in green. Important interactions of different origin are displayed with dashed black lines. The figure was created with The PyMOL Molecular Graphics System, v. 2.5.2.</p> <p><strong>Scheme 1</strong>. Preparation of the amiridine-based compounds 5a-d. Reagents and conditions: <strong>a)</strong> 2-chloroacetyl chloride (4 eq.), CHCl3, 90 ◦C, overnight, 8, 54%, 11, 90%, 12, 52%; <strong>b)</strong> CH3CN, K2CO3, KI, reflux, 3 h, 5a, 54%, 5b, 54%; <strong>c)</strong> amiridine (1.1 eq), CH3CN, K2CO3, KI, reflux, overnight, 5c, 48%, 5d, 41%.</p> <p><strong>Scheme 2</strong>. Preparation of intermediate 13 and final compound 6. Reagents and conditions: <strong>a)</strong> potassium phthalimide, CH3CN, reflux, 3 h, then an excess of NH2NH2⋅H2O, reflux, overnight, 57%; <strong>b)</strong> DMF, TEA, BOP, room temperature, 2 days, 86%.</p> <p><strong>Scheme 3</strong>. Preparation of amiridine-benzothiazole derivatives 7a-m. Reagents and conditions: <strong>a)</strong> for 7a: 2-chlorobenzothiazole, 110 ◦C, overnight, 32%; for 7b-m: corresponding 2-chlorobenzothiazole, DIPEA, 100 ◦C, overnight, 21–77%.</p>
OpenData for the Independent morphological variables correlate to aging, Mild Cognitive Impairment, and Alzheimer's Disease manuscript
<p>Results from processed structural MRI images from the <a href="https://www.sciencedirect.com/science/article/pii/S1053811920306868">AHEAD</a> and <a href="https://www.nature.com/articles/s41597-021-00870-6">AOMIC</a> dataset included in the Supplementary Information at the Independent morphological variables correlate to aging, Mild Cognitive Impairment, and Alzheimer's Disease manuscript from de Moraes et al. submitted to PNAS.</p> <p>For this data, we processed the datasets with <a href="https://surfer.nmr.mgh.harvard.edu/">FreeSurfer</a> v6.0.0 standard processing pipeline (<em>recon-all</em>) and the estimation of the <a href="https://surfer.nmr.mgh.harvard.edu/fswiki/LGI">local Gyrification Index</a> from <a href="http://ltswww.epfl.ch/~schaer/Schaer_TMI.pdf">Schaer, M. et al. 2008</a>. We further extracted the morphological measurements from the generated surfaces using the Cortical Folding Analysis Tools from <a href="https://zenodo.org/record/3608675">Wang et al. 2019</a>. Here, we included the raw morphological datasets joined with the demographics and subjects' information.</p>
# Single-cell network biology characterizes cell type gene regulation for drug repurposing and phenotype prediction in Alzheimer's disease
<p>Dysregulation of gene expression in Alzheimer’s disease (AD) remains elusive, especially at the cell type level. Gene regulatory network, a key molecular mechanism linking transcription factors (TFs) and regulatory elements to govern target gene expression, can change across cell types in the human brain and thus serve as a model for studying gene dysregulation in AD. However, it is still challenging to understand how cell type networks work abnormally under AD. To address this, we integrated single-cell multi-omics data and predicted the gene regulatory networks in AD and control for four major cell types, excitatory and inhibitory neurons, microglia and oligodendrocytes. Importantly, we applied network biology approaches to analyze the changes of network characteristics across these cell types, and between AD and control. For instance, many hub TFs target different genes between AD and control (rewiring). Also, these networks show strong hierarchical structures in which top TFs (master regulators) are largely common across cell types, whereas different TFs operate at the middle levels in some cell types (e.g., microglia). The regulatory logics of enriched network motifs (e.g., feed-forward loops) further uncover cell type-specific TF-TF cooperativities in gene regulation. The cell type networks are highly modular and several network modules with cell-type-specific expression changes in AD pathology are enriched with AD-risk genes and putative targets of approved and pending AD drugs, suggesting possible cell-type genomic medicine in AD. Finally, using the cell type gene regulatory networks, we developed machine learning models to classify and prioritize additional AD genes. We found that top prioritized genes predict clinical phenotypes (e.g., cognitive impairment) with reasonable accuracy. Overall, this single-cell network biology analysis provides a comprehensive map linking genes, regulatory networks, cell types and drug targets and reveals dysregulated cell type gene dysregulatory mechanisms in AD.</p>
Computational Investigation of Co-Aggregation and Cross-Seeding between Aβ and hIAPP Underpinning the Crosstalk in Alzheimer's Disease and Type-2 Diabetes
<p><span>The coexistence of Amyloid-β (Aβ) and human Islet Amyloid Polypeptide (hIAPP) in the brain and pancreas is associated with an increased risk of Alzheimer’s disease (AD) and type-2 diabetes (T2D) due to their co-aggregation and cross-seeding. Despite this, the molecular mechanisms underlying their interaction remain elusive. Here, we systematically investigated the cross-talk between Aβ and hIAPP using atomistic discrete molecular dynamics (DMD) simulations. Our results revealed that the amyloidogenic core regions of both Aβ (Aβ<sub>10–21</sub> and Aβ<sub>30–41</sub>) and hIAPP (hIAPP<sub>8-20</sub> and hIAPP<sub>22-29</sub>), driving their self-aggregation, also exhibited a strong tendency for cross-interaction. This propensity led to the formation of β-sheet-rich hetero-complexes, including potentially toxic β-barrel oligomers. The formation of Aβ and hIAPP hetero-aggregates did not impede the recruitment of additional peptides to grow into larger aggregates. Our cross-seeding simulations demonstrated that both Aβ and hIAPP fibrils could<a name="_Hlk163119646"></a> mutually act as seeds, assisting each other's monomers in converting into β-sheets at the exposed fibril elongation ends. The amyloidogenic core regions of Aβ and hIAPP, in both oligomeric and fibrillar states, exhibited the ability to recruit isolated peptides, thereby extending the β-sheet edges, with limited sensitivity to the amino acid sequence. These findings suggest that targeting these regions by capping them with amyloid-resistant peptide drugs may hold potential as a therapeutic approach for addressing AD, T2D, and their co-pathologies.</span></p>
Iron Trace Elements Concentration in PM10 and Alzheimer's Disease in Lima, Peru: Ecological Study - dataset
<p>This dataset was created to evaluate the association between iron trace-elements concentration in PM10 with Alzheimer´s Disease cases in different districts in Lima, Peru. The database was constructed using open-access repositories of the Peruvian Ministry of Health and the Peruvian CDC.</p> <p>The uploaded datasets are in .dta and .csv formats.</p>
Adenosine deficiency facilitates CA1 synaptic hyperexcitability in the presymptomatic phase of a mouse KI model of Alzheimer disease.
<p><span>All data points, statistical models and raw western blot images from "Adenosine deficiency facilitates CA1 synaptic hyperexcitability in the presymptomatic phase of a mouse KI model of Alzheimer disease" are available. </span></p>
BRAIN Journal-New Computer Assisted Diagnostic to Detect Alzheimer Disease-Figure 19. Accuracy of classification using the three methods: KNN, SVM and our method for MCI subjects
<p>Whatever the patient condition, Normal, MCI or AD, our method has provided us with better results. Advocate Example precision for Normal Patients was found 96% as opposed to 88% for the SVM method and 84% for KNN. For MCI patients was found 88% as opposed to 80% for the SVM method and 72% for KNN. Also for AD patients were found 92% as opposed to 88% for the SVM method and 80% for KNN. Our classification method gave us the best results, finding overall accuracy of 92% as opposed to 84% for the SVM method and 78.66% for KNN. </p>
BRAIN Journal-New Computer Assisted Diagnostic to Detect Alzheimer Disease-Figure 20. The accuracy of classification using the three methods, KNN, SVM and our method, for AD subjects
<p>Whatever the patient condition, Normal, MCI or AD, our method has provided us with better results. Advocate Example precision for Normal Patients was found 96% as opposed to 88% for the SVM method and 84% for KNN. For MCI patients was found 88% as opposed to 80% for the SVM method and 72% for KNN. Also for AD patients were found 92% as opposed to 88% for the SVM method and 80% for KNN. Our classification method gave us the best results, finding overall accuracy of 92% as opposed to 84% for the SVM method and 78.66% for KNN. </p>
BRAIN Journal-New Computer Assisted Diagnostic to Detect Alzheimer Disease-Figure 18. Accuracy of classification using the three methods, KNN, SVM and our method, for normal subjects
<p>We present three figures representing the accuracy of the classification using the three methods, KNN, SVM and our method for normal, MCI and Alzheimer subjects. </p>
BRAIN Journal-New Computer Assisted Diagnostic to Detect Alzheimer Disease-Figure 17. The results of calculating the Hausdorff distances
<p>The results of calculating the Hausdorff distances, Dice, PSNR, MSSD for the four methods<br> (Caselles Chan & Vese, Lanktom, our method) and the ground truth about a Normal subject following the<br> Corpus Calosum segmentation. </p> <p> </p>
BRAIN Journal-New Computer Assisted Diagnostic to Detect Alzheimer Disease-Figure 16. Results of calculating the Hausdorff distances
<p>Results of calculating the Hausdorff distances, Dice, PSNR, MSSD between the four methods (Caselles Chan & Vese, Lanktom, our method) and the ground truth about a subject Normal following segmentation of the Corpus Calosum.</p>
BRAIN Journal-New Computer Assisted Diagnostic to Detect Alzheimer Disease-Figure 15. The results of calculating the Hausdorff distances
<p>The results of calculating the Hausdorff distances, Dice, PSNR, MSSD for the four methods (Caselles Chan & Vese, Lanktom, our method) and the ground truth about a Normal subject following the Corpus Calosum segmentation.</p>
BRAIN Journal-New Computer Assisted Diagnostic to Detect Alzheimer Disease-Figure 14. A comparison between the results
<p> A comparison between the results. Each column shows the superposition of the corresponding results: Caselle (yellow curve), Chan & Vese (curve blue) Lankton (red curve), our method (purple line) and the ground truth (Curve Green) for a normal subject, MCI and AD.</p>
ScienceDex guides
Understand access before you commit
These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
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.