Search Existing Tissue Requests

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: 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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Investigator: 2025-001

Project Title: Leveraging a large GRN family to identify resilience factors in Frontotemporal Lobar Degeneration: a genetic and proteomic approach

Date: March 13, 2025 at 8:14 am

Request ID: T2501

Aim 1: To identify single nucleotide variants that modify disease presentation in GRN mutation carriers.

Aim 2: To identify structural variants that alter disease presentation in GRN mutation carriers

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Investigator: Yi Zhang

Project Title: How would inclusion of “low tau” subgroups impact PBO progression rate?

Date: February 20, 2025 at 3:10 pm

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Aim 1: Identify “low-tau” screen-fails above the plasma p-Tau217 low-cutoff but below the tau PET low-cutoff

Aim 2: Match these individuals to comparable individuals in studies of treatment-naïve clinical progression

Aim 3: Leverage the clinical progression data to predict PBO progression rate of these populations

Aim 4: Compare trial power change when including different % of “low tau” subgroups


Investigator: Paul Kotzbauer

Project Title: Testing the Synucleinopenia Hypothesis – Are Brain tissue Levels of Soluble Alpha-Synuclein Decreased in Parkinson Disease?

Date: December 19, 2024 at 11:23 am

Request ID: T2419 Kotzbauer

Aim 1: Determine whether levels of soluble α-syn measured in five cortical regions are lower in PD participants compared to control participants.

Aim 2: Determine whether levels of soluble α-syn correlate with levels of insoluble α-syn and also whether each of these measures correlates with motor and cognitive symptoms of PD.

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Investigator: Nicolas Barthelemy

Project Title: Unraveling the link between tau modifications, neuroinflammation and tauopathies

Date: December 13, 2024 at 5:56 pm

Request ID: T2418 Barthelemy

Aim 1: To evaluate the effect of CNS PAD enzymes on soluble and insoluble tau citrullination in brain from participants with AD and non-AD tauopathies

Aim 2: To explore potential relationship existing between brain tau abnormal phosphorylation and citrullination and evaluate how these abnormalities associate with tau aggregation in AD and non-AD tauopathies

Aim 3: To evaluate the impact of 3R+4R tau pathology on the specificity of biomarker candidate of astrocytic tau pathology

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Investigator: Partha Dutta

Project Title: The role of microglia in cognitive impairment in patients with myocardial infarction

Date: October 15, 2024 at 10:21 am

Request ID: T2417 Dutta

Aim 1: To correlate mircoglial epigenetic modifiers with cognitive functin after myocardial infarction

Aim 2: To assess hippocampal microglia-neuron crosstalk in patients with myocardial infarction

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Investigator: Hongyu AN

Project Title: Neuroinflammation in Cerebral Small Vessel Disease using PET/MR Imaging

Date: October 15, 2024 at 9:51 am

Request ID: T2302-A

Aim 1: Determine if S1PR1 expression increases and colocalizes with microglia and astrocytes in post-mortem brain specimens from deceased patients with underlying CSVD.

Aim 2: Determine if neuroinflammation measured by 11C-CS1P1 uptake is independently associated with CSVD structural endpoints using in vivo PET/MR imaging.

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Investigator: Heleen Verlinden

Project Title: Comprehensive analysis of cellular responses to Alzheimer’s and comorbid pathologies

Date: September 13, 2024 at 4:54 am

Request ID: T2416

Aim 1: To identify the cellular transcriptional changes to AD pathology in the superior frontal gyrus of postmortem human brains.

Aim 2: We aim to identify the cellular transcriptional changes to amyloid plaques without tau pathology compared to amyloid-associated tau pathology. This will help to refine the mechanism resolving amyloid stress or preventing amyloid-induced tau pathology.

Aim 3: Our overall aim is to identify new medicines to preserve cognition and other brain functions, enhance resilience to disease pathology, and slow or stop the progression of neurodegenerative diseases.

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