Search DIAN Tissue Requests
Assistant professor Henrietta M Nielsen, PhD
CSF alpha-synuclein in familial versus sporadic AD
5/24/2016
DIAN-T1604
To assess CSF alpha-synuclein levels in patients with familial AD versus sporadic AD and controls
To investigate potential associations between CSF alpha-synuclein levels, AD biomarkers (piB-PET and CSF AD biomarkers) and cognitive status in familiar AD patients
To investigate potential effects of APOE genotype on CSF alpha-synuclein levels in familial versus sporadic AD patients
Suzanne Schindler
Comparison of intra-individual change in INNOTEST CSF biomarkers in Autosomal Dominant Alzheimer Disease and Late Onset Alzheimer Disease
4/25/2016
DIAN-T1603
Aim 1: Characterization of intra-individual CSF biomarker changes
Aim 2: Correlation of CSF and imaging biomarkers of neurodegeneration
Aim 3: CSF biomarkers predict cognitive performance
Nikolaos Robakis
Role of PS1 and FAD mutants on neuronal receptor complexes.
1/25/2016
DIAN-T1602
Examine role of PS1 and FAD mutants on neuronal receptor complexes and dimerization
Examine effects of PS1 and FAD mutants on the neuroprotective activities of BDNF and ephrins
Mathias Jucker
NfL in CSF of familial AD (DIAN)
1/7/2016
DIAN-T1601
to relate CSF NfL levels to the disease progression in familial AD
Christian Haass
CSF Progranulin in autosomal dominant Alzheimer?s disease
12/24/2015
DIAN-T1506
Determine how cerebrospinal fluid (CSF) Progranulin levels change in relation to estimated years from expected symptom onset (EYO) in mutation carriers (MC) compared to non-carriers (NC)
Test whether CSF Progranulin levels are associated with cross-sectional and longitudinal changes in PIB-PET, FDG-PET, and structural MRI, rsfMRI, with other CSF biomarkers (Abeta42, T-tau, p-tau), clinical symptoms (MMSE, CDR-SOB) and cognitive performance (memory and executive functions).
Study the association of CSF Progranulin and CSF sTREM2
Eric A. Schon
Diagnosis of AD based on perturbed MAM function in fibroblasts
12/3/2015
DIAN-T1505
To test the hypothesis that Alzheimer disease can be diagnosed in fibroblasts based on the analysis of phenotypes associated with increased ER-mitochondrial communication.
Dr Charlotte Warren-Gash
HSV1 reactivation and clinical manifestation of autosomal dominant familiar Alzheimer?s disease
7/17/2015
DIAN-T1504
Overall aim: Investigate whether herpes simples virus 1 reactivation accelerates the onset or progression of dementia in individuals at risk from autosomal dominant Alzheimers disease.
Specific objectives:To measure serum IgG HSV-1 titres from serial samples collected from participants in the DIAN study
To compare rates of cognitive decline using standardised cognitive tests and quantitative brain atrophy measures in individuals with and without baseline HSV-1 IgG antibodies, using multiple linear regression models stratified by a range of potential confounders.
To assess whether the presence of IgG HSV-1 positivity results in earlier than predicted age of onset of clinical onset of AD in mutation carriers
Felix Mueller-Sarnowski
Progranuscreen - crossectional and longitudinal levels of progranulin and its relation to other markers of neurodegeneration
6/6/2015
DIAN-T1503
Crossectional and longitudinal description of progranulin levels of ADAD mutation carriers and mutation negative descendants of mutation carriers. Results are correlated with demographic, lab and imaging data.
To explore whether progranulin influences amyloid levels (blood and CSF) and amyloid deposition (shown by PIB-PET) as suggested by mouse models (Minami et al., Nature Medicine 2014).
Evaluation of progranulin as diagnostic and prognostic marker. Exploring the epidemiology of progranulin levels in different compartments of ADAD mutation carriers and healthy controls.
Identifying GRN mutation carriers as well as PGRN deficiencies that do not result from mutations for further investigations.
Randall Bateman M.D.
Dominantly Inherited Alzheimer's Disease Protective Factor Study
2/17/2015
DIAN-T1502
To have tissue samples from at least 12 related family members analyzed by the Genome Institute at Washington University School of Medicine to look for any protective factor that may account for one family member not proceeding to signs of Alzheimer's Disease 15 years over the age of onset 50
To create and administer questionnaires to at least 12 family members looking for an "incidence", "factors such as environmental" etc that may explain the existance of a protective factor in one family member.
Shauna Yuan
In-vitro clinical trial with gamma-secretase modulators for the treatment of FAD carriers
2/2/2015
DIAN-T1501
Demonstration of target engagement for different FAD mutations
Evaluation of the effects of GSMs in human induced pluripotent stem cell in-vitro systems on downstream pathways affected in AD