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: Takahisa Kanekiyo, David Holtzman, Alison Goate
Project Title: Determine apoE isoform-dependent changes incomposition of apoE lipoprotein particles in human CSF
Date: August 12, 2025 at 7:38 pm
Request ID: T2317-A
Aim 1: Purify apoE particles from human CSF samples usingantibody-based pull-down assay.
Aim 2: Assess the apoE particle size distribution with human CSFsamples.
Aim 3: Detect the apoE particles associated proteins and lipidsby proteomics and lipidomics profiling.
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Investigator: Marco Colonna
Project Title: Evaluating Vigil Neuroscience’s antibodies for their localization in brain tissue from patients with Alzheimer’s disease and cerebral amyloid angiopathy
Date: July 10, 2025 at 5:32 pm
Request ID: T2510
Aim 1: Vigil Neuroscience has developed antibodies targeting the TREM2 and its ligands. Through a sponsored research agreement, we aim to test their recognition of amyloid plaques in brain tissue from AD and CAA patients by immunohistochemistry.
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Investigator: Marijne Vandebergh
Project Title: Unravelling the genetic basis of disease penetrance and clinical heterogeneity in individuals with a pathogenic GRN mutation through omics-based approaches
Date: July 3, 2025 at 2:47 am
Request ID: T2509
Aim 1: To validate TMEM106B as modifier of disease penetrance
Aim 2: To identify novel genetic modifiers for onset age and clinical variability in individuals with FTD and GRN mutations
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Investigator: Yuna Ayala
Project Title: Aggregation and TDP-43 dysfunction are tightly linked and amplified by impaired autoregulation and Ataxin-2
Date: July 2, 2025 at 1:43 pm
Request ID: T2112-A
Aim 1: Complete revision of a manuscript characterizing mechanisms that link TDP-43 aggregation to its mislocalization and loss of function, key features of ALS, FTD, and related dementias, and highlighting the potential of targeting this link for diagnosis and intervention.
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Investigator: Yuna Ayala
Project Title: Determining the mechanism of TDP-43 aggregate seeding and loss of function
Date: June 26, 2025 at 4:29 pm
Request ID: T2507
Aim 1: Aggregate seeding by insoluble FTD brain extract triggers progressive TDP-43 loss of function in cells. We aim to define factors that modulate this process and identify TDP-43 functions most sensitive to dysfunction. A submitted manuscript was favorably reviewed, tissue is critical for revision.
Aim 2: We will define how liquid-liquid phase separation controls TDP-43 pathology. ALS-linked mutations that reduce condensate fluidity enhance aggregation and seeding. We will test whether promoting liquid-like properties inhibits seeding and define how impaired phase separation drives pathology.
Aim 3: In collaboration with Drs. T. Miller and P. Kotzbauer (Washington University), we aim to develop novel TDP-43 aggregate inhibitors and degraders to reduce pathology and preserve function, using models of aggregation and dysfunction triggered by FTD-derived proteopathic seeds.
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Investigator: Vimal Srivastava
Project Title: Therapeutic Efficacy Towards Plaque Reduction in 3D-Reprogrammed Human Alzheimer’s Disease Neurons
Date: June 12, 2025 at 4:08 pm
Request ID: T2506
Aim 1: We aim to develop a fibroblast-to-neuron transdifferentiation cell culture model for both healthy and AD-patient derived fibroblasts, under advisement by Dr. Andrew Yoo
Aim 2: We aim to evaluate our gene therapy towards reduction in amyloid plaque burden in 3D-reprogrammed neurons derived from Alzheimer’s Disease patients.
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Investigator: Gregory J. Brewer
Project Title: Redox State for AD Resilience
Date: June 4, 2025 at 5:52 pm
Request ID: T2505
Aim 1: Determine whether plasma and CSF redox states more accurately discriminate dementia than amyloid pathology. We hypothesize that a reductive redox profile is protective, while an oxidative shift contributes to dementia even with low amyloid burden.
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Investigator: Jonathan Kipnis
Project Title: Contribution of skull bone marrow-derived cells to Alzheimer’s disease
Date: May 15, 2025 at 12:31 pm
Request ID: T2504 Kipnis
Aim 1: To investigate the spatial distribution of brain-engrafting monocyte-derived macrophages in the brains of healthy and AD patients to determine if they are localized to sites of AD pathology.
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Investigator: Lien Nguyen
Project Title: Studying contribution of repeat expansions in Alzheimer’s disease
Date: April 17, 2025 at 10:21 am
Request ID: T2503
Aim 1: To test the hypothesis that repeat expansions within SINE/VNTR/Alu retrotransposable elements is associated with increased AD risk
Aim 2: To test the hypothesis that repeat expansions within SINE/VNTR/Alu retrotransposable elements contribute to AD via toxic mutant polymeric proteins
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Investigator: Gabriel Linares
Project Title: Biomarkers for synapse protection in Alzheimer’s Disease
Date: April 15, 2025 at 4:21 pm
Request ID: T2502
Aim 1: Evaluate levels of Ryk in biofluids from AD patients to determine if increased Ryk expression correlates with disease severity
Aim 2: Examine the association between Ryk expression and downstream AD pathologies
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