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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Plasma cell-free RNA as non-invasive biomarker for neurodegeneration
Validate genomic models for disease pathology in Autosomal Dominant Alzheimer
Develop a specific predictive model for ADAD
Identification and validation of novel AD biomarkers for clinical development of Eisai AD pipelines
To profile of CSF MTBR-tau isoforms which can be captured by E2814 across all DIAD stages using CSF samples from DIAN-observation cohort.
1) Dr. Alison M. Goate, 2) Dr. Sarah M. Neuner
Defining the role of microglia in Alzheimer’s disease risk and resilience
Aim 1: Investigate the effect of high-risk or protective amyloid precursor protein (APP) mutations on microglia cell function.
Optimization of a blood diagnosis of the silent phase of Alzheimer's disease
Confirm the performance of a diagnostic algorithm developed on European plasma samples.
Improve the algorithm by learning on human plasma samples of more varied genetic origin and environmental background.
Improve the algorithm by learning on human plasma samples collected longer before the diagnosis of Alzheimer's disease.
Apolipoprotein E isoform levels and their relevance to the development of AD pathology
By use of mass-spectrometry assess and compare the individual apolipoprotein E isoform levels in plasma and CSF from familial AD patients versus controls
To investigate whether fluid levels of apolipoprotein E are related to the estimated year of disease onset, CSF and imaging AD biomarkers in familial AD patients
To elucidate a potential correlation between plasma apolipoprotein E levels and previously assessed CSF alpha-synuclein levels whereof the latter appeared related to amyloid-beta deposition and symptom onset
Zlokovic, Berislav V. and Toga, Arthur W.
Blood-brain barrier dysfunction in autosomal dominant Alzheimer’s disease (ADAD)
To evaluate the effects of ADAD mutations on the molecular biomarkers of NVU and BBB dysfunction in PSEN1 and other ADAD pre-symptomatic and symptomatic MCs compared to non-MC carriers, and determine how they relate to each other, and whether NVU/BBB dysfunction can contribute to cognitive impairment and other pathologies in ADAD.
Comparison of the iPSC Characteristics between Caucasian and Asian ADAD Families
To compare charateristics of iPSCs between caucasian and asian ADAD families
Plasma Levels of an N-terminal Tau Fragment as Predictors of Cognitive Decline and Neurodegeneration in DIAN
Using cross-sectional and longitudinal plasma samples from DIAN, we will assess levels of plasma NT1 (SIMOA) and correlate these with estimated years to symptom onset (EYO), rates of neurodegeneration (MRI-based), and cognitive performance (using the DIAN global cognitive composite).
Using pre-existing measures of NfL from prior DIAN studies, we will compare and contrast the associations of plasma NfL and NT1 to cognitive and neurodegenerative trajectories.
Therapeutic development for familial Alzheimer’s disease
To determine whether therapeutic candidates can affect Abeta processing in cultured fibroblasts from autosomal dominant Alzheimer disease (ADAD) patients with PSEN1 mutations
Brain DNA methylation in Autosomal Dominant Alzheimer’s disease
Aim 1: To identify Differentially Methylated Loci (DML) in ADAD and sporadic AD and neuropath-free controls
Aim 2. To identify genetic loci modulating DML, and their downstream impact in brain transcriptomic/proteomic profiles.
Aim 3. To evaluate the causal relationship between DML and AD pathogenesis.