Background: A timely diagnosis of Alzheimer's disease (AD) is crucial to obtain more practical treatments. In this article, a novel approach using Auto-Encoder Neural Networks (AENN) for early detection of AD was proposed.
Method: The proposed method mainly deals with the classification of multimodal data and the imputation of missing data. The data under study involve the MiniMental State Examination, magnetic resonance imaging, positron emission tomography, cerebrospinal fluid data, and personal information. Natural logarithm was used for normalizing the data. The Auto-Encoder Neural Networks was used for imputing missing data. Principal component analysis algorithm was used for reducing dimensionality of data. Support Vector Machine (SVM) was used as classifier. The proposed method was evaluated using Alzheimer's Disease Neuroimaging Initiative (ADNI) database. Then, 10fold crossvalidation was used to audit the detection accuracy of the method.
Results: The effectiveness of the proposed approach was studied under several scenarios considering 705 cases of ADNI database. In three binary classification problems, that is AD vs. normal controls (NCs), mild cognitive impairment (MCI) vs. NC, and MCI vs. AD, we obtained the accuracies of 95.57%, 83.01%, and 78.67%, respectively.
Conclusion: Experimental results revealed that the proposed method significantly outperformed most of the stateoftheart methods.
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http://dx.doi.org/10.4103/jmss.JMSS_11_20 | DOI Listing |
Curr Top Behav Neurosci
January 2025
UK Dementia Research Institute Cardiff, Cardiff University, Cardiff, UK.
Mol Neurobiol
January 2025
School of Pharmacy, Nantong University, 19 Qixiu Road, Nantong, 226001, People's Republic of China.
Growing evidence suggests that plant compounds are emerging as a tremendous source for slowing the onset and progression of Alzheimer's disease (AD). Ursonic acid (UNA) is a naturally occurring pentacyclic triterpenoid with some hypoglycemic, anticancer, and antiinflammatory activities. However, the pharmacological effects of UNA on AD are still unknown.
View Article and Find Full Text PDFEur J Nucl Med Mol Imaging
January 2025
Laboratory of Neuroimaging and Innovative Molecular Tracers (NIMTlab), Geneva University Neurocenter and Faculty of Medicine, University of Geneva, Geneva, Switzerland.
Purpose: As dual-phase amyloid-PET can evaluate amyloid (A) and neurodegeneration (N) with a single tracer injection, dual-phase tau-PET might be able to provide both tau (T) and N. Our study aims to assess the association of early-phase tau-PET scans and F-fluorodeoxyglucose (FDG) PET and their comparability in discriminating Alzheimer's disease (AD) patients and differentiating neurodegenerative patterns.
Methods: 58 subjects evaluated at the Geneva Memory Center underwent dual-phase F-Flortaucipir-PET with early-phase acquisition (eTAU) and F-FDG-PET within 1 year.
J Neurol
January 2025
Alzheimer's Disease and Other Cognitive Disorders Unit, Neurology Service, Hospital Clínic de Barcelona, Fundació de Recerca Clínic - Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Universitat de Barcelona, Villaroel 170, 08036, Barcelona, Spain.
Plasma tau phosphorylated at threonine 181 (p-tau181) and 217 (p-tau217) have demonstrated high accuracy for Alzheimer's disease (AD) diagnosis, defined by CSF/PET amyloid beta (Aβ) positivity, but most studies have been performed in research cohorts, limiting their generalizability. We studied plasma p-tau217 and p-tau181 for CSF Aβ status discrimination in a cohort of consecutive patients attending an academic memory clinic in Spain (July 2019-June 2024). All patients had CSF AD biomarkers performed as part of their routine clinical assessment.
View Article and Find Full Text PDFSci Rep
January 2025
Division for Neurogeriatrics, Centre for Alzheimer Research, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden.
Copy number variation (CNV) of the amyloid-β precursor protein gene (APP) is a known cause of autosomal dominant Alzheimer disease (ADAD), but de novo genetic variants causing ADAD are rare. We report a mother and daughter with neuropathologically confirmed definite Alzheimer disease (AD) and extensive cerebral amyloid angiopathy (CAA). Copy number analysis identified an increased number of APP copies and genome sequencing (GS) revealed the underlying complex genomic rearrangement (CGR) including a triplication of APP with two unique breakpoint junctions (BPJs).
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