Search DIAN Tissue Requests
In order to avoid the situation where two investigators study the same research question, please search our database to determine if your topic has already been studied. If you find that your topic or a related topic has already been submitted, you may wish to contact the investigator to inquire about his/her 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 # (e.g. DIAN-T1004), the full request has been submitted and is either approved, disapproved or in process.
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Spatial transcriptomics on vaccinated AD brains
Identify spatial transcriptomic changes associated with Aβ vaccination
Models and therapies for Alzheimer's disease
Generate humanized models of early and advanced AD cellular pathogenesis
Use humanized models to explore a gene therapy for disease progression in AD
Assessing neurovascular interactions due to ADRD mutations
We will differentiate iPSCs with ADRD mutations versus controls into cerebral organoids and blood vessel cells. The goal is to examine the impact of the APP mutation on the organoids and blood vessel cells separately and interacting in a vascularized organoid.
The vascularized organoids will be sectioned and stained for Abeta, p-tau and the staining in different cell types will be quantified.
The conditioned medium produced by the vascularized organoids will be assessed for pathological markers and inflammatory factors.
The vascularized organoids will be dissociated for single cell -omics studies.
Ji Yeun Hur
Characterization of gamma-secretase complexes in fibroblasts and iPSCs from PS1 or PS2 FAD mutations
Characterize gamma-secretase complexes in fibroblasts and iPSCs
Characterize the gamma-secretase activity in fibroblasts and iPSCs
Bart De Strooper
the role of presenilin mutation in microglia cell states
Profiling the gamma-secretase substrate proteome in PSEN1 H163R iPSC-derived microglia.
Characterizing the transcriptional and functional phenotype of human PSEN1 H163R microglia in a humanized chimeric AD mouse model.
Functional characterization of brain circular RNAs in Alzheimer disease using induced pluripotent stem cell models
To analyze the role of circHOMER1 in AD-related molecular phenotypes using cellular models
Eain Murphy (David Butler, Co-Invesitigator)
Alzheimer’s Disease associated pathology induced by neurotropic viral infection.
Establish biomarkers and activity of SU110 and SU134 in iPSC-derived models of familial AD.
Do herpesvirus infections of neurons and glial cells produce neurodegenerative changes similar to those seen in Alzheimer’s Disease?
Assess the efficacy of anti-tau intrabodies to lower AD pathology in familial iPSC derived neurons with APP V717I iPSC mutation
Identification of mutation-specific networks: deep molecular profiling
Identification and Characterization of Cell-Specific Transposable Elements Implicated on Alzheimer Disease and Healthy Aging
To generate neuron and microglia specific ATAC-seq, CAGE-seq, DNA methylation and long-reads RNA-seq
DIAN-TU-001 Gantenerumab Open Label Extension Study
The primary objective of the DIAN-TU-001 Gant OLE (3 years study duration) is to determine if continued treatment with Gant at a target dose of 1500 mg (subcutaneous administration, every 2 weeks) can result in continued or complete removal of brain amyloid plaque using cerebral amyloid imaging by PiB PET.
The key secondary objective of the OLE is to evaluate the efficacy of Gant in reducing disease progression and will be assessed for the following key secondary efficacy outcome measures, such as CSF and plasma biomarkers.
Effects of PS1 FAD mutants on brain angiogenesis.
Examine whether VEGFR2 dimerization, VEGFR2/CTF1 peptide, VEGFR2 complexes, VE-cadherin angiogenic complexes and levels of VEGF ligand differ in human FAD brains compared to control brains.