Search DIAN Data Resource 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-D1004), the full request has been submitted and is either approved, disapproved or in process.

Displaying 141 - 150 of 319

Investigator:Nick Fox


Title:Longitudinal tau PET in dominantly inherited Alzheimer’s disease

Date of Request:07/04/2019




Aim 1:a) to understand the role tau PET imaging can play as a marker of early Alzheimer’s disease for clinical diagnostic purposes and also as a biomarker in trials of individuals with autosomal dominantly inherited forms of Alzheimer’s disease (ADAD)




Aim 2:b) to optimize static and dynamic methods of tau PET analysis in order to achieve better longitudinal consistency and reduce sources of within-subject variability




Aim 3:c) to improve understanding of when and where tau deposition occurs, and how these relationships change over time;




Aim 4d) to determine the relationship between changes in tau deposition and changes related to neurodegeneration and cognitive decline; and

Investigator:Ben Handen, Bradley Christian, William Klunk


Title:Comparing CSF biomarkers of AD in Down Syndrome and autosomal dominant AD

Date of Request:06/21/2019




Aim 1:To analyze and compare levels of established and novel CSF biomarkers (Aβ40, Aβ42, tTau, pTau, VILIP-1, Ng, SNAP-25, YKL-40, NfL, and sTREM2) between ABC-DS and DIAN cohorts.










Investigator:Randall Bateman and Gil Ribinovici


Title:Comparison between Dominant Inherit Alzheimer Disease and sporadic early-onset Alzheimer’s disease.

Date of Request:06/03/2019




Aim 1:To compare clinical presentation, neuropsychological performance and cognitive decline rate between DIAD and sporadic EOAD.




Aim 2:To examine the regional distribution of tau, amyloid-β, glucose metabolism, and structural atrophy in DIAD and sEOAD.




Aim 3:To determine CSF biomarkers levels and biomarkers rate of change in DIAD and sEOAD.




Investigator:FEI HUA


Title:Development of a robust quantitative systems pharmacology model of amyloid beta and tau pathways for clinical trial design and decision making in Alzheimer’s disease and dementia

Date of Request:05/24/2019




Aim 1:Calibrate the QSP model to longitudinal biomarker changes for different mutation status




Aim 2:Virtual patient creation to capture the patient variability




Aim 3:Predict drug treatment effect with virtual patient population




Investigator:Julia TCW


Title:Isogenic APOE isoform glia response to amyloid in brain organoids

Date of Request:05/16/2019




Aim 1:Generation of induced pluripotent stem cells from APP (and/or PS1) mutations




Aim 2:Differentiation of the iPSC to organoids to generate beta-amyloid aggregates and differentiation of isogenic APOE iPSC to microglia




Aim 3:Co-culture isogenic APOE 33 and APOE 44 microglia with the organoids from APP (and/or PS1) mutations




Aim 4Single cell transcriptomic analysis from co-cultured organoids

Investigator:NA


Title:Protective Factors in DIAN

Date of Request:05/15/2019




Aim 1:Analyze the rates of change in cognition and AD biomarkers in ADAD mutation carriers that are past expected age of onset and are not showing any symptoms










Investigator:Joana B. Pereira


Title:Alterations of the Brain Connectome in Familial Alzheimer's disease

Date of Request:05/14/2019




Aim 1:To define the changes in the structural and functional connectomes in symptomatic and asymptomatic mutation carriers with ADAD




Aim 2:To map these changes as a function of estimated years to onset of AD




Aim 3:To assess whether the connectome alterations are associated with cerebrospinal fluid and blood biomarkers, voxel-wise amyloid, tau and glucose metabolism PET, and clinical measures




Investigator:Joana B. Pereira


Title:Alterations of the Brain Connectome in Familial Alzheimer's disease

Date of Request:05/14/2019




Aim 1:To define the changes in the structural and functional connectomes in symptomatic and asymptomatic mutation carriers with ADAD




Aim 2:To map these changes as a function of estimated years to onset of AD




Aim 3:To assess whether the connectome alterations are associated with cerebrospinal fluid and blood biomarkers, voxel-wise amyloid, tau and glucose metabolism PET, and clinical measures




Investigator:Jet Vonk


Title:Cognitive markers of preclinical Alzheimer's disease through psycholinguistic semantic measures

Date of Request:05/03/2019




Aim 1:To estimate the temporality of semantic impairment in the preclinical phase of Alzheimer’s disease










Investigator:Daniel C Alexander


Title:Sequencing cognitive decline within familial AD progression

Date of Request:04/09/2019

Status:Pending

ID:DIAN-D1909




Aim 1:Construct an event-based model of cognitive decline in dominantly-inherited AD from DIAN data using a similar set of outcomes to those in [Baker–AlzDem:DADM-2017]. This will include separating subscores into cognitive domains which will allow us to validate the new technique against current thinking in neurology and neuropsychology.




Aim 2:Compare different versions of the event-based model to determine which limitations are important to address, which elements of the model are essential, which variants of the model (and its parameters/settings) are feasible, and how much complexity can be supported by different-sized data sets.




Aim 3:Extend the model to include a broader set of biomarker data including tau PET, amyloid PET, CSF (molecular changes), MRI, DTI (atrophy and microstructural changes) and other factors. This will enable cognitive decline to be positioned within the pathophysiological cascade.