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 91 - 98 of 98
DIAN-ADNI Comparison study
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
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
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.
Characterize other similarities and any differences in AD phenotypes between LOAD and ADAD
Aβ-specific fibrin fragment resistant to fibrinolysis in the CSF and plasma of familial AD patients with HCHWA
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.
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.
Human iPSC-derived organoids to study Alzheimer?s disease
to generate cortical organoids from iPSCs of AD patients and controls
to generate iPSCs from APP mutation fibroblasts
To study pathological events of AD in organoids
Dr. A Claudio Cuello
Investigating early NGF dysmetabolism as a source of novel biomarkers in ?silent? stages of Alzheimer?s disease
To investigate plasma markers of NGF dysmetabolism as a source of biomarkers in pre-clinical AD
To investigate CSF markers of NGF dysmetabolism as a source of biomarkers in pre-clinical AD
In-depth characterization of iPSC-derived neuronal models carrying familial dementia mutations
Generation and development of human neuronal models with dementia-related dysfunctions
To explore molecular mechanism of neuronal malfunctions by FAD-linked mutations
MPIs: Tom Montine and Mike MacCoss
Molecular Phenotyping in Alzheimer's Disease
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.
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.
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.
Jacques P. Tremblay
Development of a treatment of Alzheimer based on the editing of the Amyloid Precuror Protein gene with the CRISPR system
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
Investigating Cell-type dependent phenotypes in familial Alzheimer's disease
To determine if there are differential effects of neuronal subtype on APP processing with fAD mutation
To determine if there are differential effects of neuronal subtype on tau proteostasis with fAD mutation