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: Matthew R. Brier
Project Title: Immune Mechanisms of Amyloid-β Protection in Multiple Sclerosis: NULISAseq Proteomic Profiling of Non-MS Knight ADRC Controls
Date: August 24, 2026 at 11:52 am
Request ID: D2655
Aim 1: Determine whether MS modifies the plasma proteomic signature of Aβ pathology.
Aim 2: Test whether cumulative DMT exposure reduces AD biomarker burden.
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Investigator: N/A
Project Title: Multimodal Genetic, Biomarker, Neuroimaging, and Clinical Analysis of Alzheimer’s Disease and Related Dementias in the Knight ADRC Cohort
Date: August 24, 2026 at 10:14 am
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Aim 1: To characterize genetic variants, APOE genotype, and polygenic risk profiles associated with Alzheimer’s disease and related dementia diagnoses using all eligible Knight ADRC participants with available genetic and clinical data.
Aim 2: To evaluate the associations of Alzheimer’s disease, Parkinson’s disease, and frontotemporal dementia polygenic risk scores with disease status and available cognitive and clinical phenotypes.
Aim 3: To investigate the relationships between genetic factors, including APOE genotype, and cerebrospinal fluid biomarkers, including amyloid-beta 42, phosphorylated tau, and total tau.
Aim 4: To develop and evaluate integrative models combining genetic variants, polygenic risk scores, demographic variables, and available biomarkers for Alzheimer’s disease risk stratification and phenotype prediction.
Investigator: Jesus Gil Ruiz
Project Title: A cerebral vascular fragility index from structural MRI, anchored against neuropathologically confirmed cerebral amyloid angiopathy
Date: August 24, 2026 at 6:00 am
Request ID: D2654
Aim 1: Derive an imaging-based cerebral vascular fragility index from T1/T2*/SWI/FLAIR MRI, using microhaemorrhages and superficial siderosis as the trainable signal, following our established ADNI/A4 protocol.
Aim 2: Anchor the index against neuropathologically confirmed cerebral amyloid angiopathy severity (NACC Neuropathology Data Form) in participants with completed autopsy.
Aim 3: Test whether the index improves on an honest clinical baseline (APOE + age + baseline microhaemorrhage count) using out-of-bag validation with permuted-label negative controls.
Aim 4: Relate the index to longitudinal clinical outcomes (incident stroke, dementia diagnosis, mortality) and cognitive trajectories where available.
Investigator: Francesca Vitali
Project Title: Multi-Omic Signatures of Menopause and Menopausal Hormone Therapy in Alzheimer’s Disease
Date: August 20, 2026 at 5:00 pm
Request ID: D2653
Aim 1: Identify plasma and CSF proteomic, metabolomic, and transcriptomic signatures associated with menopausal status and menopausal hormone therapy use in women with NACC-linked clinical data.
Aim 2: Determine whether menopause- and hormone therapy-associated molecular signatures are related to Alzheimer’s disease biomarkers, cognitive impairment, and longitudinal cognitive decline.
Aim 3: Evaluate heterogeneity in menopause- and hormone therapy-associated multi-omic signatures by APOE genotype, age, timing of hormone therapy use, and Alzheimer’s disease clinical status.
Aim 4: Integrate multi-omic and clinical data to identify molecular pathways and druggable targets that may explain heterogeneity in the relationship between menopausal hormone therapy and Alzheimer’s disease risk.
Investigator: Wenquan Liang
Project Title: Organ Factor Research
Date: August 14, 2026 at 6:32 am
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Aim 1: Study the connections between multi-organ interactions and diseases as well as aging.
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Investigator: Jaeseung Jeong
Project Title: Multi-Omic Validation of Cognitive Resilience in Alzheimer Disease
Date: August 13, 2026 at 8:56 pm
Request ID: D2652
Aim 1: Replicate a pathology-conditioned continuous cognitive-resilience phenotype in amyloid-confirmed prodromal Alzheimer disease, with cognitively unimpaired amyloid-negative and amyloid-positive groups analyzed separately.
Aim 2: Test a frozen ADNI-derived, NPTX2-excluded CSF proteomic signature without protein reselection or reweighting, and compare its performance with NPTX2 and YWHAG:NPTX2.
Aim 3: Determine whether the resilience phenotype and frozen CSF signature predict subsequent cognitive decline, CDR-SB progression, functional impairment, and clinical transition.
Aim 4: Evaluate genetic and multi-omic support across CSF, plasma, and brain using APOE, pQTLs, transcriptomics, methylation, metabolomics, proteomics, and neuropathology.
Investigator: Gonzalo Mena
Project Title: Independent validation of a cerebrospinal-fluid endothelial activation signature for longitudinal memory decline in Alzheimer disease
Date: August 4, 2026 at 2:19 pm
Request ID: D2651
Aim 1: Test whether a prespecified CSF endothelial activation score (VCAM1, ICAM1, VWF, TIMP1, THBS1, SERPINE1) predicts subsequent memory decline independently of age, baseline cognition, amyloid, and tau.
Aim 2: Determine whether the CSF endothelial score is associated primarily with longitudinal decline rather than cross-sectional cognitive level and whether its association fades at high tau burden.
Aim 3: Evaluate whether MRI white-matter hyperintensity burden attenuates the endothelial score–decline association, consistent with small-vessel injury as a potential intermediate or shared disease feature.
Aim 4: Test specificity and robustness across cognitive domains, assay quality filters, clinical stage, sex, APOE genotype, vascular risk, and leave-one-protein-out versions of the fixed panel.
Investigator: Jiang Bian
Project Title: OmniBioTwin: An AI-Enabled, System-of-SystemsDigital Twin for Multi-Scale Mechanistic Modeling
Date: August 3, 2026 at 4:06 am
Request ID: D2650
Aim 1: Identify longitudinal clinical, cognitive, biomarker, and neuroimaging features associated with cognitive decline and progression from normal cognition to MCI or dementia.
Aim 2: Develop and validate interpretable multimodal machine-learning models to predict cognitive decline, incident MCI, dementia, and disease progression.
Aim 3: Evaluate the incremental predictive value of MRI, PET, CSF, blood biomarkers, and genetic risk factors beyond demographic and clinical measures.
Aim 4: Characterize distinct longitudinal trajectories and examine model performance across demographic, clinical, and disease-severity subgroups.
Investigator: NA
Project Title: Characterizing fluid biomarkers in atypical tau PET subtypes
Date: July 29, 2026 at 2:39 pm
Request ID: D2649
Aim 1: Test whether fluid biomarkers of pTau isoforms, MTBR, inflammatory processes, and neurodegeneration consistently associate with amyloid beta across distinct tau stubtypes.
Aim 2: Test whether fluid biomarkers of pTau isoforms, MTBR, inflammatory processes, and neurodegeneration consistently associate with tau PET across distinct tau stubtypes.
Aim 3: Test whether fluid biomarkers of pTau isoforms, MTBR, inflammatory processes, and neurodegeneration consistently associate with dementia status across distinct tau stubtypes.
Aim 4: Test whether fluid biomarkers of pTau isoforms, MTBR, inflammatory processes, and neurodegeneration consistently associate with cognition across distinct tau stubtypes.
Investigator: Maurizio Giorelli
Project Title: Alzheimer Disease instability score in predicting clinical tipping point
Date: July 28, 2026 at 5:24 am
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Aim 1: To build a multifactorial clinical instability score which may help to follow the longitudinal course of patient
Aim 2: To compare values from cognitively normal and clinical converter so to uncover if a real clinical significance exist for this score
Aim 3: To evaluate the course of this score six continuos clinical visits in either normal and converter to evaluate if changes in score predict clinical conversion
Aim 4: To buil table of values related to age and AD so allowing point by point evaluation in clinical practice