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.
Displaying 1 - 10 of 87
Jee Hoon Roh/Jae-Hong Lee
Epigenetic analyses to assess the resilience among DIAN mutation carriers
To investigate the potential epigenetic causes of resilience among DIAN mutation carriers who are discordant in disease courses measured by biomarkers.
Multi-Omics CSF and plasma signature of ADAD
To identify ADAD-specific multi-omic (proteomics and metabolomic) signatures CSF and plasma
To identify multi-omic (metabolomics and proteomics) plasma signatures and QTLs in ADAD
High-resolution multiplex localization of Alzheimer’s disease risk and resilience factors
Determine the expression levels, localization, and co-localization patterns of proteins in the m109 and BIN1 protein clusters in relation to synaptic markers. Synaptic changes have long been recognized to be tightly linked to AD severity (9). We will determine the expression patterns of the two protein clusters relative to excitatory and inhibitory synapses using antibodies specific for excitatory synapses (e.g., AMPA- and NMDA-type receptors and PSD-95), inhibitory synapses (e.g., vesicular GABA transporter/VGAT and gephyrin), and presynaptic terminals (e.g., synapsin).
Determine the expression levels, localization, and co-localization patterns of proteins in the m109 and BIN1 protein clusters in relation to AD pathology. Probable AD is confirmed at autopsy by the presence of amyloid plaques and tangles (10). We will determine the expression patterns of the two protein clusters as a function of proximity to regions with amyloid plaques (using a 6E10 antibody), neurofibrillary tangles (using a tau13 antibody), astrocytes (using a GFAP antibody), and microglia (using an Iba1 antibody).
Capturing the mitochondrial complexity in familial Alzheimer's disease
Use high-content and high-throughput assays to quantify the MT dynamics phenotypes that develop in neurons derived from iPSCs of fAD subjects compared to age-matched and/or isogenic controls.
Define the functional impairment in these neurons (IMM-inner mitochondrial membrane potential).
Interrogate the function of the electron transport chain (ETC) in these neurons.
Measure the structural integrity of MT, the ETC, and MT-related processes in these neurons by quantitative Western blotting of proteins
Randall J Bateman
Comprehensive analyses of the soluble microtubule binding region (MTBR)in Alzheimer disease progression.
The Primary Aim of this study isto identify which tau species are novel and different inthe novelUCB vs. other antibodies which have been used to characterize the soluble tau in CSF of DIAN(e.g. Tau1 or E2814).
The stage of the disease where additional MTBRisoforms begin to differ between MC and NC based on EYO and Aβ status andcompare this to the recently identified MTBR and p-tau mass spec measures of MTBR tau and p-tau.
The longitudinal change (quantitative change / mean and SD) of thenovel MTBRfragmentsas it relates to disease stage and how this compares to the recently identified MTBR and p-tau mass specmeasures of MTBR tau and p-tau.
The association between regional NFT tau burden (post-mortem) and MTBR (based on the novel antibody and Eisai antibody) to assess for the correlation between soluble and insoluble fractions of MTBR with AD related NFTs. Design:
Mariah S. Hahn
Targeting Dysregulated Synapse and Proteostasis Mechanisms in Alzheimer's Disease
Develop a 3D culture system compatible with long-term (>3 month) iNeuron culture, extension, synapse formation and elimination, and quantitative assessment of neural circuit activity using “healthy” networks.
Compare AD_(PSEN1)-iNeuron cultures to iNeuron cultures derived from unaffected family member controls with respect to Aβ, tau phosphorylation, synapse maintenance and proteostasis.
Molecular detection of α-synuclein co-pathology in ADAD mutation carriers
Use real time quaking induced conversion (RT-QuIC) for ante mortem detection of Synuclein pathology in ADAD mutation carriers
Compare the data from RT-QuIC regarding in vivo detection of Synuclein pathology with data from post mortem examinations (manuscript in preparation).
Within the time frame of 15 years EYO we will analyse the time-point of emergence of LB pathology as measured by RT-QuIC .
We will analyse clinical and imaging data longitudinally comparing RT-QuIC positive and RT-QuIC negative participants.
VE-cadherin in Alzheimer Disease
Examine the diagnostic value of CSF and plasma levels of VE-cadherin as a marker of vascular injury in EOAD
Investigate whether VE-cadherin correlates with CSF and imaging measures of amyloid, tau, brain atrophy, and glucose hypometabolism in EOAD in cross-sectional and longitudinal analyses
Determine whether baseline VE-cadherin levels influences age of onset or rate of cognitive decline in asymptomatic and symptomatic mutation carriers
Metabolomic and lipidomics changes in ADAD
Determine metabolite signatures of ADAD
Identify locus-metabolite and lipids associations via Metabolite genome-wide association studies (M-GWAS).
Measurement of glial fibrillary acidic protein (GFAP) levels in blood for evaluation of astrocyte reaction in Alzheimer disease.
Determine trajectory of GFAP over the ADAD disease course in relation to amyloid