DIAN Data Resource Requests

Title:Association of b-amyloid accumulation and cognitive decline in healthy older adults : a systematic review and meta-analysis

Date of Request:05/27/2021

ID:DIAN-D2108

Aim 1:Systematic review and meta-analysis of selected articles studying the longitudinal association between amyloid accumulation and cognitive decline in preclinical Alzheimer's disease (in cognitively healthy older adults)

Aim 2:Obtain data from the following article : Simultaneously evaluating the effect of baseline levels and longitudinal changes in disease biomarkers on cognition in dominantly inherited Alzheimer’s disease

Title:Characterization of the Neuroinflammation in Autosomal Dominant Alzheimer Disease Using Neuro-Inflammation Imaging

Date of Request:04/26/2021

ID:DIAN-D2107

Aim 1:Determine the trajectory of NII neuroinflammation biomarkers during the natural course of AD in the DIAN cohort.

Aim 2:Examine the association between whole-brain NII neuroinflammation biomarkers and CSF inflammation measures (sTREM2 and YKL40) in the DIAN cohort.

Aim 3:Assess the relationships among neuroinflammation measured by NII, amyloid deposition, and tauopathy measured by PET tracers in the DIAN cohort.

Title:Plasma biomarkers in Autosomal Dominant AD

Date of Request:03/31/2021

Status:Approved

ID:DIAN-D2106

Aim 1:Aim 1a: Determine whether plasma markers of amyloid (i.e., Ab42, Ab42/40) at baseline predict current and future CSF and PET markers of amyloid. Aim 1b: Assess longitudinal changes in plasma amyloid in relation to changes in CSF and PET amyloid.

Aim 2:Aim 2a: Determine whether plasma markers of tau (i.e., t-tau, p-tau181) at baseline predict current and future CSF and PET markers of tau. Aim 2b: Assess longitudinal changes in plasma tau in relation to changes in CSF and PET tau.

Aim 3:Aim 3a: Determine if the combination of plasma amyloid and tau markers at baseline predict current and future downstream markers (i.e., neurodegeneration [MRI], cognitive performance, and clinical status [clinical dementia rating (CDR) sum of boxes] in ADAD. Aim 3b: Assess longitudinal changes in plasma amyloid and tau in relation to changes in downstream markers of neurodegeneration and cognitive status.

Title:Using quantitative traits to identify new genes, biomarkers and drug targets for ADAD and LOAD

Date of Request:09/08/2020

Status:approved

ID:DIAN-D2018

Aim 1:To identify genetic variants associated with biomarker levels and quantitative traits in ADAD

Aim 2:To identify novel variants and genes associated with onset and progression by using multi-omics QTL data

Aim 3:To identify novel molecular biomarkers and drug targets by combining multi-omic QTL and Mendelian randomization analysis

Title:Imaging White matter hyperintensities and Tau in Autosomal Dominant Alzheimer’s Disease

Date of Request:09/04/2020

ID:DIAN-D2017

Aim 1:To determine the difference in the relationship among tau and WMH, independent or dependent on amyloid, between mutation carriers and controls.

Aim 2:To characterize the timing of the relationship among tau and WMH in mutation carriers compared to controls.

Aim 3:To characterize any added benefit to incorporating spatial information from tau PET in Aims 1 and 2.

Aim 4To determine the difference in the relationship among baseline WMH and tau accumulation between mutation carriers and controls.

Title:Specific facets of Personality traits in Autosomal Dominant Alzheimer disease

Date of Request:08/30/2020

Status:approved

ID:DIAN-D2016

Aim 1:1) to determine the different baseline differences between mutation carriers and non-mutation carriers in respect to the facets within each Personality Factor (OCEAN: openness to experience, conscientiousness, extraversion, agreeableness, and neuroticism). 2) to analyze longitudinal changes of facets within mutation-carriers and non-carriers.

Title:Investigating microRNA and immune gene regulation in fAD gene carriers

Date of Request:07/30/2020

Status:approved

ID:DIAN-D2015

Aim 1:To determine if AD pathogenesis involves altered gene regulation of peripheral macrophage function, we will profile miRNA/mRNA expression in monocytes isolated from ADAD gene carriers or age-matched controls. We hypothesize that dysregulated peripheral immune cells in ADAD further contribute to disease. In collaboration with the Wash U DIAN site, we have collected CD14 cells from DIAN participants. We will use computational approaches to characterize the impact of ADAD mutations on peripheral cells. We include DIAN collected variables for analyses.

Title:Functional connectivity disruptions at early stages in Alzheimer’s Disease: a comparison of brain networks in mouse models and humans.

Date of Request:07/20/2020

Status:approved

ID:DIAN-D2014

Aim 1:We would like to access rsfMRI data from APP and PSEN1/2 carriers versus non carriers to compare functional connectivity disruptions in human AD with functional connectivity disruptions we observe in mouse models of Alzheimer's pathology. We would like to compare whether the same brain regions are involved, to study the extent to which our findings in mice can be translated to humans.

Title:Neurological examination findings in Alzheimer disease

Date of Request:06/22/2020

Status:approved

ID:DIAN-D2013

Aim 1:to determine a muster of neurological examination findings in AD and to investigate their prevalences over the disease course

Aim 2:evaluate the capability of neurological examinations findings in Alzheimer disease to distinguish mutation carriers from non mutation carriers among mildly cognitive symptomatic at risk individuals

Aim 3:to analyze cross-sectional and

Aim 4longitudinal associations between cognitive performance and neurological examination findings in Alzheimer disease

Title:Functional and Structural Correlates of Genetics in ADAD

Date of Request:06/15/2020

ID:DIAN-D2012

Aim 1:Does connectivity strength change based on APOE status or associate with the polygenetic risk score in an ADAD cohort.

Aim 2:Does structural connectivity change based on APOE status or associate with the polygenetic risk score in an ADAD cohort.

Aim 3:Does structural or functional connectivity temporally associate with proteomic data.