House defense bill would vastly expand requirements.
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http://dx.doi.org/10.1126/science.adj8306 | DOI Listing |
Neurobiol Aging
December 2024
Center for Lifespan Changes in Brain and Cognition, Department of Psychology, University of Oslo, Oslo 0373, Norway.
Structural brain changes underlie cognitive changes and interindividual variability in cognition in older age. By using structural MRI data-driven clustering, we aimed to identify subgroups of cognitively unimpaired older adults based on brain change patterns and assess how changes in cortical thickness, surface area, and subcortical volume relate to cognitive change. We tested (1) which brain structural changes predict cognitive change (2) whether these are associated with core cerebrospinal fluid (CSF) Alzheimer's disease biomarkers, and (3) the degree of overlap between clusters derived from different structural modalities in 1899 cognitively healthy older adults followed up to 16 years.
View Article and Find Full Text PDFEBioMedicine
January 2025
Department of Neurosurgery, Stanford University, Stanford, CA, USA.
Background: Perivascular spaces (PVS) on brain MRI are surrogates for small parenchymal blood vessels and their perivascular compartment, and may relate to brain health. However, it is unknown whether PVS can predict dementia risk and brain atrophy trajectories in participants without dementia, as longitudinal studies on PVS are scarce and current methods for PVS assessment lack robustness and inter-scanner reproducibility.
Methods: We developed a robust algorithm to automatically assess PVS count and size on clinical MRI, and investigated 1) their relationship with dementia risk and brain atrophy in participants without dementia, 2) their longitudinal evolution, and 3) their potential use as a screening tool in simulated clinical trials.
Genome Med
December 2024
Department of Biostatistics, Boston University School of Public Health, Boston, MA, USA.
bioRxiv
September 2023
Helen Wills Neuroscience Institute, University of California, Berkeley, Berkeley, CA, USA.
Amyloid-β (Aβ) and tau deposition constitute Alzheimer's disease (AD) neuropathology. Cortical tau deposits first in the entorhinal cortex and hippocampus and then propagates to neocortex in an Aβ-dependent manner. Tau also tends to accumulate earlier in higher-order association cortex than in lower-order primary sensory-motor cortex.
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