Catastrophic forgetting, which means a rapid forgetting of learned representations while learning new data/samples, is one of the main problems of deep neural networks. In this paper, we propose a novel incremental learning framework that can address the forgetting problem by learning new incoming data in an online manner. We develop a new incremental learning framework that can learn extra data or new classes with less catastrophic forgetting. We adopt the hippocampal memory process to the deep neural networks by defining the effective maximum of neural activation and its boundary to represent a feature distribution. In addition, we incorporate incremental QR factorization into the deep neural networks to learn new data with both existing labels and new labels with less forgetting. The QR factorization can provide the accurate subspace prior, and incremental QR factorization can reasonably express the collaboration between new data with both existing classes and new class with less forgetting. In our framework, a set of appropriate features (i.e., nodes) provides improved representation for each class. We apply our method to the convolutional neural network (CNN) for learning Cifar-100 and Cifar-10 datasets. The experimental results show that the proposed method efficiently alleviates the stability and plasticity dilemma in the deep neural networks by providing the performance stability of a trained network while effectively learning unseen data and additional new classes.
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http://dx.doi.org/10.3390/s23198117 | DOI Listing |
Brain Struct Funct
January 2025
Department of Biomedical Engineering, College of Chemistry and Life Sciences, Beijing University of Technology, Beijing, 100124, China.
The brain undergoes atrophy and cognitive decline with advancing age. The utilization of brain age prediction represents a pioneering methodology in the examination of brain aging. This study aims to develop a deep learning model with high predictive accuracy and interpretability for brain age prediction tasks.
View Article and Find Full Text PDFActa Neuropathol
January 2025
Department of Neurology, NYU Grossman School of Medicine, New York, NY, USA.
Down syndrome (DS) is strongly associated with Alzheimer's disease (AD) due to APP overexpression, exhibiting Amyloid-β (Aβ) and Tau pathology similar to early-onset (EOAD) and late-onset AD (LOAD). We evaluated the Aβ plaque proteome of DS, EOAD, and LOAD using unbiased localized proteomics on post-mortem paraffin-embedded tissues from four cohorts (n = 20/group): DS (59.8 ± 4.
View Article and Find Full Text PDFLangmuir
January 2025
Department of Physics and Astronomy, The University of Tennessee, Knoxville, Tennessee 37996, United States.
Biological memory is the ability to develop, retain, and retrieve information over time. Currently, it is widely accepted that memories are stored in synapses (i.e.
View Article and Find Full Text PDFJ Chem Theory Comput
January 2025
Preferred Networks, Inc., Tokyo 100-0004, Japan.
Mapping the chemical reaction pathways and their corresponding activation barriers is a significant challenge in molecular simulation. Given the inherent complexities of 3D atomic geometries, even generating an initial guess of these paths can be difficult for humans. This paper presents an innovative approach that utilizes neural networks to generate initial guesses for reaction pathways based on the initial state and learning from a database of low-energy transition paths.
View Article and Find Full Text PDFJ Neurochem
January 2025
Center for Protein Diagnostics (PRODI) Biospectroscopy, Ruhr University Bochum, Bochum, Germany.
Alzheimer's disease (AD) is characterized by the accumulation of amyloid-beta (Aβ) plaques in the brain, contributing to neurodegeneration. This study investigates lipid alterations within these plaques using a novel, label-free, multimodal approach. Combining infrared (IR) imaging, machine learning, laser microdissection (LMD), and flow injection analysis mass spectrometry (FIA-MS), we provide the first comprehensive lipidomic analysis of chemically unaltered Aβ plaques in post-mortem human AD brain tissue.
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