The Knight ADRC has supported many investigators at Washington University and at other institutions over the years. We wish to avoid the situation where two investigators study the same research question to avoid duplication of effort and potential conflict. To determine if your topic has already been studied with our resources, please search our database. If you find that your topic or a related topic has been submitted, you may wish to contact the investigator to inquire about their findings to determine how you might proceed. You may wish to collaborate or modify your request to avoid overlap. The results below reflect requests made since online requests have been accepted. As such, not all fields will have data as certain information, such as aims, were not collected until recently. If an entry has been assigned an ID number (e.g. T1004), the full request has been submitted and is either approved, disapproved or in process. If an entry has no ID number, then it represents a submission that has not yet been reviewed. Search terms are applied across an entire requests application including variables not displayed below. A more specific, detailed search may yield better results depending upon your needs.
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Investigator: Andrew J. Aschenbrenner
Project Title: Clarifying the role of mind wandering in Alzheimer disease
Date: July 9, 2025 at 11:49 am
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Aim 1: Determine if subjective and objective mind wandering metrics from the new tasks sensitive to amyloid burden cross-sectionally
Aim 2: Determine if the amyloid to mind wandering relationship depend upon clinical status (CDR 0 vs. CDR 0.5).
Aim 3: Determine if mind wandering moderates the relationship between amyloid and standard cognitive outcomes (e.g., the Knight Preclinical Alzheimer Disease Cognitive Composite (PACC)).
Aim 4: Determine if mind wandering correlates with other clinical outcomes.
Investigator: Lukai Zheng
Project Title: Uncovering distinct spatial-temporal trajectories of tau accumulation to predict disease progression and cognition decline in Alzheimer’s disease
Date: July 2, 2025 at 8:19 pm
Request ID: D2527
Aim 1: To determine whether tau-PET defined AD subtypes can predict longitudinal amyloid and tau accumulation, as well as cognition decline in individuals across the AD spectrum.
Aim 2: To test if there is a sex-specific effect of tau-PET defined subtypes on tau spreading and cognition decline.
Aim 3: To develop and evaluate a ML model that predicts longitudinal cognitive performance based on baseline multimodal data.
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Investigator: Andy Qi
Project Title: Alzheimer’s Disease Plasma Proteomics Study
Date: June 25, 2025 at 1:30 pm
Request ID: D2526
Aim 1: Build machine learning models to predict AD based on proteomic data.
Aim 2: Validate biomarkers in independent cohorts to ensure reproducibility.
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Investigator: Jonathan Kipnis
Project Title: Contribution of blood- vs skull-derived immune cells to Alzheimer’s disease – Brase et al study
Date: June 13, 2025 at 2:14 pm
Request ID: D2525
Aim 1: Analyze snRNAseq data from Knight ADRC samples from the dataset published in Brase, et al. Single-nucleus RNA-sequencing of autosomal dominant Alzheimer disease and risk variant carriers (https://doi.org/10.1038/s41467-023-37437-5) to compare against a mouse derived gene s
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Investigator: Cruchaga
Project Title: Identification of cortical and blood circular RNA in Alzheimer’s Disease
Date: June 12, 2025 at 8:13 pm
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Aim 1: 1. To benchmark the blood circRNA models in predicting AD compared to MS tau analytes in CSF and plasma.
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Investigator: Anna-Lena Schubert
Project Title: Monitoring Cognition in the Wild
Date: June 11, 2025 at 8:22 am
Request ID: D2524
Aim 1: This project aims to evaluate the psychometric properties and temporal dynamics of smartphone-based cognitive assessments in older adults, using data from Project 4 of the Health Aging and Senile Dementia (HASD) study.
Aim 2: First, it seeks to inform design parameters for future longitudinal ecological momentary assessment (EMA) studies.
Aim 3: Second, it aims to investigate idiographic dynamics in cognitive functioning.
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Investigator: Eric McDade
Project Title: Proteostasis markers in Alzheimer disease biomarker and clinical progression
Date: June 5, 2025 at 5:19 pm
Request ID: D2523
Aim 1: 1. To explore CSF levels of proteasome related peptides across the AD biomarker progression (Core 1 (-)/Core 2 (-), Core 1 (+)/Core 2 (-), Core 1 (+)/Core 2 (+)).
Aim 2: 2. Evaluate the association of proteasome related peptides with biomarkers of soluble and aggregated forms of amyloid ß and tau, neurodegeneration and microglia.
Aim 3: 3. Assess the ability of UPS vs autophagy-lysosome peptides in predicting longitudinal tau-PET, neurodegeneration and clinical progression.
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Investigator: Philip B. Verghese
Project Title: Establishing Concordance Between the PrecivityAD2™ Blood Test and FDA-Approved CSF Biomarkers to Support Regulatory Submission for AD Diagnosis
Date: June 1, 2025 at 8:31 am
Request ID: D2522
Aim 1: To evaluate the concordance between the PrecivityAD2™ blood test and FDA-cleared Lumipulse CSF β-Amyloid 1-42/1-40 ratio test in individuals with cognitive impairment.
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Investigator: Private Funding for Teal Omics
Project Title: Expanding Organ- and Cell-Specific Aging Models to Understand Aging in Health and Diseases
Date: May 28, 2025 at 2:58 pm
Request ID: D2521
Aim 1: Extend aging models to more organs and cell types than initially published
Aim 2: Study how proteome-based organ- and cell-specific aging measures are influenced by health status
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Investigator: Xiaoping Gu
Project Title: Validation of YWHAG as a Novel Biomarker for Perioperative Neurocognitive Disorders Using Knight-ADRC Plasma Proteomics Data
Date: May 21, 2025 at 11:27 pm
Request ID: D2520
Aim 1: To validate the association between YWHAG protein levels and cognitive impairment using Knight-ADRC plasma proteomic data.
Aim 2: To compare the expression patterns of YWHAG in perioperative cognitive impairment and Alzheimer’s disease cohorts.
Aim 3: To explore the correlation of YWHAG with clinical cognitive scores and other established biomarkers.
Aim 4: To identify potential interacting pathways involving YWHAG that contribute to neurodegeneration.