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.
Search Terms:
Investigator: David Holtzman
Project Title: Validation of novel human apoE antibody staining in human AD and CAA tissue
Date: [208]
Request ID: T1921
Aim 1: To determine whether a novel anti-human apoE antibody with therapeutic potential binds amyloid plaques in human AD and CAA tissue
Aim 2: To quantify the proportion of anti-human apoE antibody binding to apoE in parenchymal plaques compared to CAA
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Investigator: Gilbert Gallardo
Project Title: Targeting Reactive Astrocytes for Therapeutic Intervention of Alzheimer�s Disease
Date: [208]
Request ID: T1920
Aim 1: The purpose of this tissue request is to test our hypothesis that the astrocytic α2-NKA and related genes are elevated in Alzheimer�s disease patients.
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Investigator: Gregory J. Zipfel
Project Title: Impact and Mechanisms of Vascular Oxidative Stress on CAA Pathogenesis and CAA-Related Dementia
Date: [208]
Request ID: T1919
Aim 1: Correlate HSPG expression with NADPH oxidase activity, vascular oxidative stress, altered LRP1 and oxidized-LRP1 levels, and CAA in cerebral vessels of Alzheimer’s and non-Alzheimer’s autopsy samples
Aim 2: Correlate NADPH oxidase activity with vascular oxidative stress, altered LRP1 and oxidized-LRP1 expression, and CAA load in cerebral vessels of Alzheimer’s and non-Alzheimer’s autopsy samples
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Investigator: Ron DeMattos
Project Title: Analyses of Full-Length, Truncated, and Modified Aβ Species across the Alzheimer�s Disease Spectrum
Date: [208]
Request ID: T1408-A
Aim 1: Extend previous study to include a biochemical and histological evaluation of the same tissues for Tau and neuroinflammatory pathology
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Investigator: Timothy Miller
Project Title: Identifying the impact of increased 4R tau in human astrocytes
Date: [208]
Request ID: T1918
Aim 1: Examine changes in gene and protein expression in various tauopathies.
Aim 2: Identify morphological differences in astrocytes from autopsy samples.
Aim 3: Identify how 4R tauopathies differ from mixed tauopathies.
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Investigator: Berislav Zlokovic
Project Title: T1234_WashU ADRC:CSF BIOMARKERS OF BLOOD-BRAIN BARRIER BREAKDOWN IN COGNITIVELY NORMAL AND ALZHEIMER�S INDIVIDUALS WITH DIFFERENT APOE GENOTYPES
Date: [208]
Request ID: T1917
Aim 1: To determine the effects of APOE genotype on CSF biomarkers of BBB breakdown e.g., CypA, MMP-9, albumin quotient and pericyte marker PDGFRb in cognitively normal younger and older individuals, and correlate these markers with established biomarkers of AD pathology and peripheral biomarkers.
Aim 2: To determine the effects of APOE genotype on CSF biomarkers of BBB breakdown e.g., CypA, MMP-9, albumin quotient and pericyte marker PDGFRb in mild and severe AD patients, and correlate these markers with established biomarkers of AD pathology and peripheral biomarkers.
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Investigator: Jermaine Ross, PhD
Project Title: Studying the correlation between potential blood-based AD biomarker and cortical gene expression
Date: [208]
Request ID: T1916
Aim 1: We aim to validate a potential biomarker for late-onset AD using matched human blood and brain samples from patients and controls.
Aim 2: We will then assess how levels in the periphery relate to observations in the brain.
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Investigator: Randall Bateman
Project Title: A blood test for symptomatic Alzheimer disease
Date: [208]
Request ID: T1915
Aim 1: Estimating the likelihood that an individual has symptomatic AD dementia based on plasma Aβ42/Aβ40 and personal characteristics (age, sex, years of education, APOE ε4 genotype, race, comorbidities).
Aim 2: For individuals who are cognitively normal, estimating the likelihood that they will develop AD dementia based on plasma Aβ42/Aβ40 and personal characteristics (age, sex, years of education, APOE ε4 genotype, race, comorbidities)
Aim 3: To determine whether inclusion of plasma NfL data (when available) will improve the models (significantly higher ROC AUC)
Aim 4: To determine the difference in diagnostic accuracy provided by CSF versus plasma.
Investigator: Richard Gross
Project Title: Mitochondrial-mediated Signaling and Neuroinflammation in Alzheimer’s Disease
Date: [208]
Request ID: T1914
Aim 1: Identification of the roles of mitochondrial phospholipases in the onset and progression of ADRD.
Aim 2: Determination of the role of cytochrome c-mediated plasmalogenase activity in mitochondrial dysfunction during ADRD.
Aim 3: Identification of the molecular species and amounts of eicosanoid-lysolipids in human brain and their alterations during the onset and progression of ADRD.
Aim 4: Identification of the biologic roles of eicosanoid-lysolipids in mitochondrial-mediated inflammation.
Investigator: Yuka A. Martens
Project Title: Pathogenic mechanism of Alzheimer-associated TREM2 variants
Date: [208]
Request ID: T1913
Aim 1: Investigate cellular dysfunctions associated with TREM2 mutations using patient-derived iMGL
Aim 2: Identify the molecular pathways affected by TREM2 mutations.
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