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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Soluble TREM2 in autosomal dominant Alzheimer’s disease
Determine whether and how many years before the estimated time point of symptom onset (EYO), mutation carriers (MC) of autosomal dominant Alzheimerâs disease (ADAD) show altered cerebrospinal fluid (CSF) and plasma levels of soluble TREM2 (sTREM2) compared to non-mutation carriers (NC).
Test whether differences in CSF and plasma levels of sTREM2 are associated with longitudinal changes in PIB-PET, FDG-PET, and structural MRI, rsfMRI, with other CSF biomarkers (AÃ42, T-tau, p-tau), clinical symptoms (MMSE, CDR-SOB) and cognitive performance (memory and executive functions).
Insulin and glucose levels in autosomal dominant Alzheimer's Disease
To measure fasting blood insulin and glucose levels in non-carriers, asymptomatic carriers, and symptomatic carriers
Relate alterations in insulin and glucose to biomarkers of AD pathology drawn from CSF, PET, and structural imaging
Identification of mutation-specific networks
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
Paul Thompson, Ph.D.
Growth factors, neuroinflammation, exercise, and brain integrity
Determine how ADAD and APOE genetic status influence inflammation markers homocysteine, TNFα, BDNF, IGF-1, VEGF, Complement Factor H, SOD1, IL-13, and CCL1 relate to brain volume.
Determine how our ROI volumes relate to measures of exercise and how growth factors and TNFα modulate any relationship between exercise and these ROIs
Effects of FAD PSEN1 mutations in mouse and human brains
To identify transcriptional alterations in sporadic and familial AD brains
In-vitro clinical trial with gamma-secretase modulators for the treatment of FAD carriers
Demonstration of target engagement for different FAD mutations
Evaluation of the effects of GSMs in human induced pluripotent stem cell in-vitro systems on downstream pathways affected in AD
Randall Bateman M.D.
Dominantly Inherited Alzheimer's Disease Protective Factor Study
To have tissue samples from at least 12 related family members analyzed by the Genome Institute at Washington University School of Medicine to look for any protective factor that may account for one family member not proceeding to signs of Alzheimer's Disease 15 years over the age of onset 50
To create and administer questionnaires to at least 12 family members looking for an "incidence", "factors such as environmental" etc that may explain the existance of a protective factor in one family member.
Progranuscreen - crossectional and longitudinal levels of progranulin and its relation to other markers of neurodegeneration
Crossectional and longitudinal description of progranulin levels of ADAD mutation carriers and mutation negative descendants of mutation carriers. Results are correlated with demographic, lab and imaging data.
To explore whether progranulin influences amyloid levels (blood and CSF) and amyloid deposition (shown by PIB-PET) as suggested by mouse models (Minami et al., Nature Medicine 2014).
Evaluation of progranulin as diagnostic and prognostic marker. Exploring the epidemiology of progranulin levels in different compartments of ADAD mutation carriers and healthy controls.
Identifying GRN mutation carriers as well as PGRN deficiencies that do not result from mutations for further investigations.
Dr Charlotte Warren-Gash
HSV1 reactivation and clinical manifestation of autosomal dominant familiar Alzheimer?s disease
Overall aim: Investigate whether herpes simples virus 1 reactivation accelerates the onset or progression of dementia in individuals at risk from autosomal dominant Alzheimers disease.
Specific objectives:To measure serum IgG HSV-1 titres from serial samples collected from participants in the DIAN study
To compare rates of cognitive decline using standardised cognitive tests and quantitative brain atrophy measures in individuals with and without baseline HSV-1 IgG antibodies, using multiple linear regression models stratified by a range of potential confounders.
To assess whether the presence of IgG HSV-1 positivity results in earlier than predicted age of onset of clinical onset of AD in mutation carriers
Eric A. Schon
Diagnosis of AD based on perturbed MAM function in fibroblasts
To test the hypothesis that Alzheimer disease can be diagnosed in fibroblasts based on the analysis of phenotypes associated with increased ER-mitochondrial communication.