A5023677212- Alzheimer's disease research and treatments
- Dementia and Cognitive Impairment Research
- Metabolomics and Mass Spectrometry Studies
- Nutritional Studies and Diet
- Bioinformatics and Genomic Networks
- Angiogenesis and VEGF in Cancer
- Memory and Neural Mechanisms
- Neurological Disease Mechanisms and Treatments
- Neurological Disorders and Treatments
Stanford University
2020-2024
Neurosciences Institute
2023-2024
Abstract Animal studies show aging varies between individuals as well organs within an individual 1–4 , but whether this is true in humans and its effect on age-related diseases unknown. We utilized levels of human blood plasma proteins originating from specific to measure organ-specific differences living individuals. Using machine learning models, we analysed 11 major estimated organ age reproducibly five independent cohorts encompassing 5,676 adults across the lifespan. discovered nearly...
Abstract Background Post‐mortem and neuroimaging studies have established the amygdala as one of earliest sites tau deposition neurofibrillary tangles. We investigated cognitive anatomical consequences levels in healthy, older adults. Method examined 226 cognitively unimpaired ADNI participants who underwent AV‐1451 PET imaging (Aß‐ = 145, Aß+ 81). identified (memory, executive functioning) MMSE scores — well neuroanatomical measures closest proximity to participants’ respective scans...
Abstract INTRODUCTION In this study, we leverage proteomic techniques to identify communities of proteins underlying Alzheimer's disease (AD) risk among clinically unimpaired (CU) older adults. METHODS We constructed a protein co‐expression network using 3869 cerebrospinal fluid (CSF) quantified by SomaLogic, Inc., in cohort participants along the AD clinical spectrum. then replicated an independent CU adults and related these modules clinically‐relevant outcomes. RESULTS discovered enriched...
Abstract Background Vascular dysfunction, blood‐brain barrier (BBB) dysregulation, and neuroinflammation are thought to participate in Alzheimer`s disease (AD) pathogenesis, though the mechanism is poorly understood. Among pathways of interest, AD pathology appears affect vascular endothelial growth factor‐A (VEGFA) signaling a bidirectional manner. Higher VEGF levels have protective role slow cognitive decline. Neuronal intracellular adhesion molecules (ICAMs) may also be marker BBB...