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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Longitudinal changes of the microglia activity markers sTREM2 and Progranulin in CSF of Dominantly Inherited Alzheimer’s disease
To determine longitudinal changes in CSF sTREM2 and CSF PGRN levels across the range of EYO.
To determine the association between baseline levels of CSF sTREM2 and CSF PGRN and their rate of change with longitudinal cognition, brain structure and metabolism at different stages of ADAD
Assess the cross-sectional association between CSF sTREM2 or CSF PGRN and AV1451 PET across different EYO.
Role of amylin in AD
Test the hypothesis that the ratio of serum amylin to CSF amylin levels increases in fAD compared to age-matched cognitively normal individuals.
Test the hypothesis that amylin interacts with Abeta to form mixed amylin-Abeta oligomers within CSF and serum in patients with fAD. We propose to measure the levels of mixed Abeta-amylin oligomers within CSF and serum in patients with fAD versus age-matched cognitively normal individuals.
Identification of mutation-specific networks. Amended
To generate RNA-seq data from brain tissue from DIAN participants (mutation carriers and non-carriers)
To identify genes differentially expressed or spliced in mutation carriers vs LOAD, and vs controls
To identify gene and mutation-specific networks and pathways
Lipidomics study of preclinical plasma biomarkers for Alzheimer´s disease
Establish a preclinical biomarker for AD
Determine lipid profiles in preclinical AD
Compare lipid profiles in DIAN and Framingham
Determine longitudinal changes of lipid profiles during disease
AD pathology in advanced cellular models
Generation of iPSCs from AD patient fibroblasts
Differentiation of AD iPSCs into neurons
Analysis of cellular networks dysfunction
Leptin and metabolic signaling in autosomal dominant Alzheimer’s disease
To determine if alterations in levels of plasma leptin and related metabolic markers are evident in cognitively normal subjects with autosomal dominant Alzheimer’s disease
To determine if alterations in plasma leptin levels and related metabolic markers correlate with changes in Alzheimer’s disease biomarkers in subjects with autosomal dominant Alzheimer’s disease
To determine if levels of plasma leptin and related metabolic markers correlate with worsening Alzheimer’s disease biomarkers and progression of cognitive decline over time (age) in subjects with autosomal dominant Alzheimer’s disease
Steve Wagner, Ph.D.
Preclinical validation of target engagement for a potent disease modifying therapeutic for AD in dominantly inherited EOFAD patient induced human neurons
Demonstrate target engagement against human neurons harboring EOFAD mutations
Evaluation of the effects of GSMs in hiPSC in-vitro systems on downstream AD pathways
DIAN-ADNI comparison study
In LOAD and ADAD determine whether both groups demonstrate initial cerebral amyloidosis that is followed by the development of neurodegeneration prior to onset of AD symptoms
Characterize similarities and any differences in AD phenotypes between LOAD and ADAD
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
Examine the contribution of age to the dementing process.
Genetic architecture of CSF biomarker levels in ADAD
To identify genetic variants and genes associated with CSF biomaker levels in DIAN
To determine the overlap in the genetic architecture of late-onset sporadic AD with ADAD
To identify protective and modifiers variants for AD
Characterization of γ-Secretase in fibroblasts derived from FAD patients harboring PSEN1or PSEN2 mutations
Determine in vitro γ-secretase activity for Aβ40 and Aβ42 production using fibroblast cell membranes
Characterize the γ-secretase complexes in fibroblast cell membranes
Examine the sensitivity of various modulators and inhibitors to γ-secretase in fibroblast cell membranes