Neuroimaging has made it possible to measure pathological brain changes associated with Alzheimer's disease (AD) in vivo. Over the past decade, these measures have been increasingly integrated into imaging signatures of AD by means of classification frameworks, offering promising tools for individualized diagnosis and prognosis. We reviewed neuroimaging-based studies for AD and mild cognitive impairment classification, selected after online database searches in Google Scholar and PubMed (January, 1985-June, 2016). We categorized these studies based on the following neuroimaging modalities (and sub-categorized based on features extracted as a post-processing step from these modalities): i) structural magnetic resonance imaging [MRI] (tissue density, cortical surface, and hippocampal measurements), ii) functional MRI (functional coherence of different brain regions, and the strength of the functional connectivity), iii) diffusion tensor imaging (patterns along the white matter fibers), iv) fluorodeoxyglucose positron emission tomography (FDG-PET) (metabolic rate of cerebral glucose), and v) amyloid-PET (amyloid burden). The studies reviewed indicate that the classification frameworks formulated on the basis of these features show promise for individualized diagnosis and prediction of clinical progression. Finally, we provided a detailed account of AD classification challenges and addressed some future research directions.
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http://dx.doi.org/10.1016/j.neuroimage.2017.03.057 | DOI Listing |
Ann Neurol
January 2025
Research Unit of Neurology, Neurophysiology and Neurobiology, Department of Medicine and Surgery, Università Campus Bio-Medico di Roma, Rome, Italy.
Objective: Despite diagnostic criteria refinements, Parkinson's disease (PD) clinical diagnosis still suffers from a not satisfying accuracy, with the post-mortem examination as the gold standard for diagnosis. Seminal clinicopathological series highlighted that a relevant number of patients alive-diagnosed with idiopathic PD have an alternative post-mortem diagnosis. We evaluated the diagnostic accuracy of PD comparing the in-vivo clinical diagnosis with the post-mortem diagnosis performed through the pathological examination in 2 groups.
View Article and Find Full Text PDFJ Imaging Inform Med
January 2025
Faculty of Mathematics and Information Science, Warsaw University of Technology, Warsaw, Poland.
Analysis of the symmetry of the brain hemispheres at the level of individual structures and dominant tissue features has been the subject of research for many years in the context of improving the effectiveness of imaging methods for the diagnosis of brain tumor, stroke, and Alzheimer's disease, among others. One useful approach is to reliably determine the midline of the brain, which allows comparative analysis of the hemispheres and uncovers information on symmetry/asymmetry in the relevant planes of, for example, CT scans. Therefore, an effective method that is robust to various geometric deformations, artifacts, varying noise characteristics, and natural anatomical variability is sought.
View Article and Find Full Text PDFBrain Inform
January 2025
Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, 02114, USA.
Cognitive resilience (CR) describes the phenomenon of individuals evading cognitive decline despite prominent Alzheimer's disease neuropathology. Operationalization and measurement of this latent construct is non-trivial as it cannot be directly observed. The residual approach has been widely applied to estimate CR, where the degree of resilience is estimated through a linear model's residuals.
View Article and Find Full Text PDFEur Radiol
January 2025
Chulalongkorn University Biomedical Imaging Group, Department of Radiology, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
Commun Med (Lond)
January 2025
Rare Disease Translational Center, The Jackson Laboratory, Bar Harbor, ME, USA.
Background: Multiple Sulfatase Deficiency (MSD) is a rare inherited lysosomal storage disorder characterized by loss of function mutations in the SUMF1 gene that manifests as a severe pediatric neurological disease. There are no available targeted therapies for MSD.
Methods: We engineered a viral vector (AAV9/SUMF1) to deliver working copies of the SUMF1 gene and tested the vector in Sumf1 knock out mice that generally display a median lifespan of 10 days.
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