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.

Displaying 101 - 109 of 109

Investigator:

Mathias Jucker

Title:

Neurofilament light chain in blood serum as marker of disease progression in neurodegenerative diseases

Date of Request:

6/29/2016

ID:

DIAN-T1606

Aim 1:

Determine whether and how many years before the estimated time point of symptom onset (EYO) mutation carriers (MC) of autosomal dominant Alzheimer?s disease (ADAD) show altered blood (serum) levels of neurofilament light chain (NfL) compared to non-mutation carriers (nMC).

Aim 2:

Test whether serum levels of NfL are correlated with previous measured CSF levels and are associated with longitudinal changes in PIB-PET, FDG-PET, and structural MRI, resting state fMRI, with other CSF biomarkers, clinical symptoms and performance

Investigator:

Randall Bateman

Title:

DIAN-ADNI Comparison study

Date of Request:

7/19/2016

ID:

DIAN-T1607

Aim 1:

characterize the stages of preclinical AD with amyloid PET and cerebrospinal fluid (CSF) concentrations of Aβ and tau and phosphorylated tau (p-tau) and determine whether both groups demonstrate initial cerebral amyloidosis that is followed by the development of neurodegeneration prior to onset of A

Aim 2:

In both ADAD and LOAD, determine whether initial symptoms of AD are characterized by subjective reports (self-reported and those of a study partner) of the gradual onset of memory impairment as well as by deficits in objective measures of episodic memory

Aim 3:

In both LOAD and ADAD, determine whether there is a pattern of disease progression that is marked by intra-individual global cognitive and functional decline that culminates in death.

Aim 4:

Characterize other similarities and any differences in AD phenotypes between LOAD and ADAD

Investigator:

Sidney Strickland

Title:

Aβ-specific fibrin fragment resistant to fibrinolysis in the CSF and plasma of familial AD patients with HCHWA

Date of Request:

9/7/2016

ID:

DIAN-T1608

Aim 1:

Analyze the level of fibrin degradation products in the antemortem CSF of HCHWA patients and compare levels to sporadic AD cases and non-demented controls.

Aim 2:

Analyze the level of an A?-specific fibrin fragment resistant to fibrinolysis in the plasma of AD patients with HCHWA and compare levels to sporadic AD cases and non-demented controls.

Investigator:

Alice PEBAY

Title:

Human iPSC-derived organoids to study Alzheimer?s disease

Date of Request:

9/9/2016

ID:

DIAN-T1609

Aim 1:

to generate cortical organoids from iPSCs of AD patients and controls

Aim 2:

to generate iPSCs from APP mutation fibroblasts

Aim 3:

To study pathological events of AD in organoids

Investigator:

Dr. A Claudio Cuello

Title:

Investigating early NGF dysmetabolism as a source of novel biomarkers in ?silent? stages of Alzheimer?s disease

Date of Request:

9/23/2016

ID:

DIAN-T1610

Aim 1:

To investigate plasma markers of NGF dysmetabolism as a source of biomarkers in pre-clinical AD

Aim 2:

To investigate CSF markers of NGF dysmetabolism as a source of biomarkers in pre-clinical AD

Investigator:

Hideyuki Okano

Title:

In-depth characterization of iPSC-derived neuronal models carrying familial dementia mutations

Date of Request:

9/30/2016

ID:

DIAN-T1611

Aim 1:

Generation and development of human neuronal models with dementia-related dysfunctions

Aim 2:

To explore molecular mechanism of neuronal malfunctions by FAD-linked mutations

Investigator:

MPIs: Tom Montine and Mike MacCoss

Title:

Molecular Phenotyping in Alzheimer's Disease

Date of Request:

10/21/2016

ID:

DIAN-T1612

Aim 1:

We will collect proteomics data on post-mortem brain samples using a liquid chromatography-tandem mass spectrometry (LC-MS/MS) strategy called data independent acquisition.

Aim 2:

Leverage high-dimensional proteomics data to identify and understand the molecular signatures of three groups that will enable precision medicine for AD: (i) different genetic risk, (ii) common co-morbidities, and (iii) resilience to AD neuropathologic change.

Aim 3:

We will make our data available through a novel cloud based solution, called the Chorus Project (http://chorusproject.org), engineered to enable big data reanalysis by the community of scientists.

Investigator:

Jacques P. Tremblay

Title:

Development of a treatment of Alzheimer based on the editing of the Amyloid Precuror Protein gene with the CRISPR system

Date of Request:

10/24/2016

ID:

DIAN-T1613

Aim 1:

To correct the APP gene in 293T cells and in Alzheimer cells with a pair of gRNA (targeting sequences in intron 15 or 16) and with dCas9-FokI

Investigator:

Young-Pearse

Title:

Investigating Cell-type dependent phenotypes in familial Alzheimer's disease

Date of Request:

12/27/2016

ID:

DIAN-T1701

Aim 1:

To determine if there are differential effects of neuronal subtype on APP processing with fAD mutation

Aim 2:

To determine if there are differential effects of neuronal subtype on tau proteostasis with fAD mutation