DIAN Tissue Resource 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.
Displaying 1 - 10 of 98
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.
Ralph A. Nixon
PSEN FAD mutation effects on autophagy-lysosomal pathway related gene regulation
Transcriptomic analysis of PSEN1 FAD mutations
Transcriptomic analysis of PSEN2 FAD mutations
Stanford Alzheimer's Disease Research CenterAdmin Supp: Developing iPSC modelsfor AD and PD
AD/ADRD phenotypic characterization of iPSC neurons and microglia. Aim 2.1: We will differentiate and characterize cell lines into cortical neurons and microglia using established and validated protocols. Aim 2.2: We will characterize cell cultures and media supernatant for established AD biomarkers, including total tau, phosphorylated tau (Thr181), A1-40, and A1-42, neurofilament light (NfL), alpha-synuclein, cytokines and chemokines, immune profiling with CYTOF, proteomics, and comparative analyses to cerebrospinal fluid (CSF) biomarkers from the same donor.
Comprehensive analyses of the soluble microtubule binding region (MTBR) in Alzheimer disease progression
To test the performance of a pharma partner's antibody to identify unique soluble tau MTBR epitopes
Quantification of Neuroinflammation in Autosomal Dominant Alzheimer's Disease Using Small-block Brain Specimen imaged by Diffusion Basis Spectrum Imaging (DBSI)
to assess the value of DBSI for the study of ADAD by comparing post-mortem MRI signals with histologic data
Investigation of plasma Beta-Synuclein levels in asymptomatic and symptomatic autosomal dominant Alzheimer´s disease
To investigate if blood levels of the synaptic marker Beta-Synuclein are already elevated in asymptomatic ADAD
To estimate a time course of blood Beta-Synuclein changes in ADAD based on EYO and comparison with other blood/CSF biomarkers
Relationship of blood Beta-Synuclein levels in ADAD with other fluid and imaging biomarkers, brain atrophy and cognitive impairment
Antonio Boza Serrano
Galectin-3 as a prognostic biomarker to monitor Autosomal dominant Alzheimer's Disease's progression
We aim to evaluate if gal3 levels are elevated in ADAD and if they might track the progression of AD pathology.
We want to compare the levels of gal3 with the levels of the classic biomarkers (amyloid-beta 42, total tau, p-tau (181, 217, etc), neurofilaments, precuneus SURV and PIB-Pet) as well as with global cognitive test (MMSE) and clinical measures (CDR total and SB) scores from the DIAN-obs