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Patient stratification by genetic risk in Alzheimer's disease is only effective in the presence of phenotypic heterogeneity.
PLoS One
January 2025
Washington University School of Medicine, NeuroGenomics and Informatics Center, St. Louis, MO, United States of America.
Case-only designs in longitudinal cohorts are a valuable resource for identifying disease-relevant genes, pathways, and novel targets influencing disease progression. This is particularly relevant in Alzheimer's disease (AD), where longitudinal cohorts measure disease "progression," defined by rate of cognitive decline. Few of the identified drug targets for AD have been clinically tractable, and phenotypic heterogeneity is an obstacle to both clinical research and basic science.
View Article and Find Full Text PDFBackground: Alzheimer's disease (AD), a complex and polygenic disease with a considerable hereditary component (60-80%), is a progressive neurodegenerative disorder characterized by concealed onset, and individuals often have significant cognitive impairment and histopathological changes in the brain before overt clinical diagnosis. However, the correlations between genetic risk for Alzheimer's disease (AD) with comprehensive brain regions at a regional scale are still not well understood. We aim to explore whether these associations vary across different age stages.
View Article and Find Full Text PDFBiomarkers.
Alzheimers Dement
December 2024
Washington University in St. Louis School of Medicine, St. Louis, MO, USA.
Background: Brain-predicted age estimates are used to quantify an individual's brain age compared to a normative trajectory. We have recently shown that brain age from structural MRI is elevated in autosomal dominant Alzheimer disease (ADAD), a unique sample that allows the study of AD progression independently of age-related confounds. Resting-state functional connectivity (FC) may capture a biphasic response to sporadic AD, and thus may complement structural measures of brain aging in ADAD.
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Alzheimers Dement
December 2024
Washington University in St. Louis School of Medicine, St. Louis, MO, USA.
Background: Alzheimer disease (AD) related cognitive decline occurs at relatively young ages in individuals with Down syndrome (DS, early-mid 50s) and in those with autosomal dominant mutations (ADAD, 40-50s). Both groups show similar patterns of amyloid accumulation. We examined if brain volumes are similarly affected by AD pathology in individuals with DS and ADAD.
View Article and Find Full Text PDFBiomarkers.
Alzheimers Dement
December 2024
University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Background: Vascular pathology associated with small vessel disease (SVD), such as microinfarcts and microbleeds, are common in elderly populations and significant contributors to cognitive impairment and dementia. Autosomal dominant cerebral arteriopathy with subcortical infarctions and leukoencephalopathy (CADASIL), caused by mutations in the Notch3 gene, is the most prominent inheritable SVD, with a common etiology of subcortical strokes and dementia. This study aimed to investigate additive or synergistic effects of CADASIL-related vascular alterations and familial Alzheimer's disease (FAD)-related amyloid pathology on cerebral metabolism of glucose and disease progression in a novel FAD-CADASIL mouse model.
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