Although existing reconstruction-based multivariate time series anomaly detection (MTSAD) methods have shown advanced performance, most assume the training data is clean. When faced with noise or contamination in training data, they can also reconstruct the anomaly well, weakening the distinction between normal and anomaly. Some probabilistic generation-based methods have been used to address this issue because of their implicit robust structure to noise, but the training process and suppression of anomalous generalization are not stable. The recently proposed explicit method based on the memory module would also sacrifice the reconstruction effect of normal patterns, resulting in limited performance improvement. Moreover, most existing MTSAD methods use a single fixed-length window for input, which weakens their ability to extract long-term dependency. This paper proposes a robust multi-scale feature extraction framework with the dual memory module to comprehensively extract features fusing different levels of semantic information and lengths of temporal dependency. First, this paper designs consecutive neighboring windows as inputs to allow the model to extract local and long-term dependency information. Secondly, a dual memory-augmented encoder is proposed to extract global typical patterns and local common features. It ensures the reconstruction ability of normal data while suppressing the generalization of the anomaly. Finally, this paper proposes a multi-scale fusion module to fuse latent variables representing different levels of semantic information and uses the reconstructed latent variables to reconstruct samples for anomaly detection. Experimental results on five datasets from diverse domains show that the proposed method outperforms 16 typical baseline methods.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.neunet.2024.106395 | DOI Listing |
PLoS One
January 2025
NCCA, Bournemouth University, Poole, United Kingdom.
Medical volume data are rapidly increasing, growing from gigabytes to petabytes, which presents significant challenges in organisation, storage, transmission, manipulation, and rendering. To address the challenges, we propose an end-to-end architecture for data compression, leveraging advanced deep learning technologies. This architecture consists of three key modules: downsampling, implicit neural representation (INR), and super-resolution (SR).
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Mount Sinai Center for Transformative Disease Modeling, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Background: Alzheimer's disease (AD) is a progressive neurodegenerative disease that inflicts the elderly worldwide. Recent studies revealed the association of abnormal methylomic alterations in AD. However, a systematic and comprehensive study is needed to investigate the effects of methylomic changes on the molecular networks underpinning AD, in particular, in brain regions most vulnerable to AD neuropathology.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
The Taub Institute for Research on Alzheimer's Disease and The Aging Brain, Columbia University, New York, NY, USA.
Background: At least one-third of the identified risk alleles from Genome Wide Association Studies of Alzheimer's disease (AD) are involved in lipid metabolism, lipid transport, or direct lipid binding. BIN1 which is also known as Amphiphysin 2; and PICALM which are involved in phosphoinositide metabolism and binding rank just below the highest risk gene variant of Apolipoprotein E (ApoEε4), a cholesterol and phospholipid transporter. In addition to genetic variants, lipidomic studies have reported severe metabolic dysregulation in human autopsy brain tissue, CSF, blood and multiple mouse models of AD.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Institute for Memory Impairments and Neurological Disorders (MIND), Irvine, CA, USA.
Background: Alzheimer's Disease (AD) presents a significant challenge in understanding its complex pathophysiology, owing to its multifaceted genetic and environmental factors. Despite extensive research, the translatability of findings from animal models to human conditions remains a critical hurdle. This study addresses the need to uncover shared molecular changes in AD by comparing human and mouse models, thereby enhancing our understanding of the disease's underlying mechanisms and improving the prospects for effective treatments.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Washington, School of Medicine, Seattle, WA, USA.
Background: Previously, we developed a co-calibrated and harmonized brain pathology score (BPS) across prospective cohort studies with research brain donation that incorporates multiple forms of postmortem neuropathology, using confirmatory factor analysis. We sought to identify genetic loci associated with BPS using a systems-biology approach, combining data from participants in the Adult Changes in Thought (ACT), the Religious Orders Study, and Rush Memory and Aging Project (ROSMAP) autopsy cohorts.
Method: We used PLINK in each cohort separately for genome-wide association studies (GWAS) of BPS using HRC imputed data from European ancestry participants, adjusting for age at death, sex, and population substructure.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!