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 11 - 20 of 104
Ralph A. Nixon
PSEN FAD mutation effects on autophagy-lysosomal pathway related gene regulation
Transcriptomic analysis of PSEN1 FAD mutations
Transcriptomic analysis of PSEN2 FAD mutations
Stanford Alzheimer's Disease Research CenterAdmin Supp: Developing iPSC modelsfor AD and PD
AD/ADRD phenotypic characterization of iPSC neurons and microglia. Aim 2.1: We will differentiate and characterize cell lines into cortical neurons and microglia using established and validated protocols. Aim 2.2: We will characterize cell cultures and media supernatant for established AD biomarkers, including total tau, phosphorylated tau (Thr181), A1-40, and A1-42, neurofilament light (NfL), alpha-synuclein, cytokines and chemokines, immune profiling with CYTOF, proteomics, and comparative analyses to cerebrospinal fluid (CSF) biomarkers from the same donor.
Comprehensive analyses of the soluble microtubule binding region (MTBR) in Alzheimer disease progression
To test the performance of a pharma partner's antibody to identify unique soluble tau MTBR epitopes
Quantification of Neuroinflammation in Autosomal Dominant Alzheimer's Disease Using Small-block Brain Specimen imaged by Diffusion Basis Spectrum Imaging (DBSI)
to assess the value of DBSI for the study of ADAD by comparing post-mortem MRI signals with histologic data
Investigation of plasma Beta-Synuclein levels in asymptomatic and symptomatic autosomal dominant Alzheimer´s disease
To investigate if blood levels of the synaptic marker Beta-Synuclein are already elevated in asymptomatic ADAD
To estimate a time course of blood Beta-Synuclein changes in ADAD based on EYO and comparison with other blood/CSF biomarkers
Relationship of blood Beta-Synuclein levels in ADAD with other fluid and imaging biomarkers, brain atrophy and cognitive impairment
Antonio Boza Serrano
Galectin-3 as a prognostic biomarker to monitor Autosomal dominant Alzheimer's Disease's progression
We aim to evaluate if gal3 levels are elevated in ADAD and if they might track the progression of AD pathology.
We want to compare the levels of gal3 with the levels of the classic biomarkers (amyloid-beta 42, total tau, p-tau (181, 217, etc), neurofilaments, precuneus SURV and PIB-Pet) as well as with global cognitive test (MMSE) and clinical measures (CDR total and SB) scores from the DIAN-obs
Study of endolysosomal alterations (including exosomes) in brain cells cultures derived from fDA iPSC lines and isogenic controls
Determine the effect of mutant APP on exosome dynamics in CNS cells in human AD models.
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).