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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Prof. Ralph Martins
Investigating blood and CSF lipid biomarkers in autosomal dominantly inherited Alzheimer's disease.
Identify early modifications in plasma, CSF and platelet lipid profiles of DIAN participants which may reveal critical information about the pathobiological cascade that culminates in symptomatic disease.
Demonstrate any correlation that may exist across the two major macromolecule subclasses in the blood and CSF, i.e. lipids and selected proteins (Aβ, ApoE, phospho and total tau) and also contribute to a panel of biomarkers to detect AD through a blood test.
Correlate the DIAN lipid profile with brain imaging data obtained from MRI, FDG-PET and PiB-PET scans and determine whether there exists a link between biochemical alterations occurring in the periphery and brain.
Development and characterization of iPS derived cellular model for Alzheimer's Disease
We are a group working on the molecular and functional characterization of neuropsychiatric illness using patient specific cellular models. LCl lines from the DIAN repository are fully characterized and would serve as informative control in our attempts to model disease phenotypes.
Marc I. Diamond
Seeding of Tau Aggregation: A Novel Plasma and CSF Biomarker for Alzheimer’s Disease
1) To determine the sensitivity and specificity of our seeding assay for identifying subjects with AD.
2) To determine when in the course of the disease process the seeding assay becomes positive.
3) To examine how seeding activity correlates with validated biomarkers in a well-studied population.
Defining the mechanisms of AD pathogenesis in human IPSC-derived neurons
To measure the influence of pathogenic FAD mutations on APP and tau metabolism in human neurons
John M. Ringman, M.D., M.S.
Metabolic profiling of biofluids in Alzheimer's Disease
Identify the compounds in the combined gas chromatography-mass spectrometry profiles that differentiate the samples collected from patients carrying and not carrying causative FAD mutations. Further analyses will compare presymptomatic and symptomatic persons carrying FAD mutations.
Identify peaks in the combined liquid chromatography-mass spectrometry profiles that differentiate samples collected from causative FAD mutation carriers and non-carriers, and presymptomatic and symptomatic FAD mutation carriers and identify the responsible compounds.
Establish and apply quantitative assays to the compounds identified in Aims 1 and 2.
Integrate all the compounds that are identified in Aims 1 and 2 into a biochemical overview, and rationalize these data with the extant knowledge about Alzheimer's Disease pathology.
Richard J. Perrin
Quantitative label-free proteomics for CSF Biomarkers in Dominantly Inherited AD
To evaluate and map the temporal patterns of novel CSF biomarkers, measured in DIAN samples using quantitative label-free proteomics. Data will be aligned according to expected symptom onset; values from carriers (N=120) and non-carriers (N=80) will be compared (as in Bateman RJ, et al. NEJM 2012).
To integrate proteomics data into the context of known AD-associated changes for this cohort (Bateman RJ, NEJM 2012), to compare novel and existing markers, and to compare this autosomal dominant dataset to a sporadic AD dataset already derived from proteomic analysis of a Knight ADRC cohort.
Karen H. Ashe
Specific CSF Abeta oligomers in unimpaired DIAN subjects
Compare CSF Abeta*56 and Abeta trimer levels in unimpaired carriers and non-carriers
Correlate CSF Abeta oligomers with Abeta1-42, tau and p-tau181
Relate CSF Abeta*56 and Abeta trimer levels to predicted age of onset
Ajay Verma MD Ph.D., VP, Development Sciences Biogen Idec
Proposal to evaluate the prognostic and diagnostic potential of selected AD biomarkers using plasma and CSF samples from DIAN registry
Evaluate total pyroglutamate-Aβ(pE3-Aβ) in plasma and CSF and other selected amyloid Aβ isoforms in CSF as prognostic/diagnostic markers of AD in symptomatic and pre-symptomatic populations of mutation carriers and non-carriers in the DIAN registry
Evaluate the CSF sTREM2 and VLP-1 markers as prognostic/diagnostic markers of AD in symptomatic and pre-symptomatic populations of mutation carriers and non-carriers in the DIAN registry
Evaluate the selected modified by oxidative stress tyrosine moieties in CSF as markers linked to amyloidogenesis, inflammation, and neuronal injury
Publish the findings from the above evaluations and share the results with Alzheimer’s disease research community
DIAN TU Biomarker Core Validation Testing
To develop and validate a method of measuring biomarker kit lot variability and new lot acceptance criteria
To establish and verify our internal quality control (QC) process for assay plate and sample acceptance criteria
To test DIAN TU drug interference on the ability of the AlzBio3 assay to detect CSF tau and ptau181
To validate the DIAN TU internal CSF pools as suitable internal controls to be used for Incurred Sample Reanalysis (ISR) during the trial
Antibody Signature of Alzheimer's Disease
To confirm whether AD has a specific and reproducible antibody signature that can be used as diagnostic test
Confirm that patients with PSEN-1 mutations have an Alzheimer-type signature
Determine whether PSEN-2 and APP mutation carrieres have an Alzheimer signature
Determine whether Alzheimer signature is present before the onset of dementia in mutation carriers