The Knight ADRC has supported many investigators at Washington University and at other institutions over the years. We wish to avoid the situation where two investigators study the same research question to avoid duplication of effort and potential conflict. To determine if your topic has already been studied with our resources, please search our database. If you find that your topic or a related topic has been submitted, you may wish to contact the investigator to inquire about their 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 number (e.g. T1004), the full request has been submitted and is either approved, disapproved or in process. If an entry has no ID number, then it represents a submission that has not yet been reviewed. Search terms are applied across an entire requests application including variables not displayed below. A more specific, detailed search may yield better results depending upon your needs.
Search Terms:
Investigator: Mohammad Moshahid Khan
Project Title: DNA double-strand breaks: A new therapeutic target for AD and AD-related dementia
Date: [208]
Request ID: T1816
Aim 1: To determine if DSBs accumulation is correlated with the severity of AD-like pathology.
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Investigator: Erik Johnson/Allan Levey
Project Title: A Proteomic Network Comparison of Autosomal Dominant and Sporadic Alzheimer�s Disease
Date: [208]
Request ID: T1815
Aim 1: Compare the brain protein network alterations that characterize autosomal dominant AD with those observed in sporadic early-onset AD
Aim 2: Compare the brain protein network alterations that characterize early-onset AD with those observed in sporadic late-onset AD
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Investigator: Terrance T Kummer
Project Title: Synaptic imaging in AD
Date: [208]
Request ID: T1814
Aim 1: characterize anatomical context of synapse loss in AD (neuropil layers, regional specificity)
Aim 2: characterize subtype specificity of synapse loss in AD (excitatory-inhibitory, receptor subtypes, etc.)
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Investigator: Randall Bateman
Project Title: A blood isotope labeled amyloid-beta test for Alzheimer’s disease
Date: [208]
Request ID: T1710-A
Aim 1: To replicate findings in a separate cohort that plasma Abeta concentrations (specifically Abeta42 and Abeta42/40 ratio) as measured by the Bateman lab N15 mass spectrometry protocol to determine sensitivity and specificity to identify amyloidosis.
Aim 2: To replicate findings in a younger cohort with moderate risk (25%-35% risk of amyloid deposition as measured by amyloid PET) of amyloidosis as measured by the Bateman lab N15 mass spectrometry protocol to determine sensitivity and specificity to identify amyloidosis.
Aim 3: If aims 1 and 2 are successful, then plans to determine longitudinal change of the plasma Abeta biomarker will be undertaken to assess stability and rate of change of the plasma Abeta biomarker.
Aim 4: If all the above aims are successful, in order to further validate a potential plasma biomarker, we request EDTA plasma and CSF samples that were collected at the same time, which are not included in aims 1-3
Investigator: Kotzbauer Paul
Project Title: Protein Aggregation in Parkinson Disease
Date: [208]
Request ID: T1813
Aim 1: To quantify the deposition of fibrillar alpha-synuclein (Asyn), Amyloid-beta (Aβ) and tau in basal ganglia, limbic and neocortical regions in Parkinson Disease (PD)
Aim 2: Relate the levels of fibrillar Aβ and tau deposited across brains regions in PD cases to the levels of these proteins in Alzheimer�s disease (AD) cases
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Investigator: Dr. David Holtzman
Project Title: Investigating the role of TREM2 mediated microgliosis in the progression of tau pathology in Alzheimer’s Disease
Date: [208]
Request ID: T1702-A Ulrich
Aim 1: We will investigate in TREM2 mutations associated with Alzheimer’s Disease leads to increased neuritic dystrophy
Aim 2: We will investigate if increased neuritic dystrophy due to TREM2 deficiency accelerates the seeding of tau pathology
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Investigator: Yinsheng Wang
Project Title: To assess the implications of alkylated and oxidative stress-induced DNA adducts in the etiology of Alzheimer’s disease
Date: [208]
Request ID: T1811
Aim 1: To assess the correlation between the levels of oxidative stress-induced DNA adducts and the levels of severity of Alzheimer’s disease
Aim 2: To assess the correlation between the levels of alkylated DNA adducts and the levels of severity of Alzheimer’s disease
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Investigator: Amber Southwell
Project Title: Investigating the mechanism(s) of release of huntingtin protein to cerebrospinal fluid
Date: [208]
Request ID: T1810
Aim 1: Measure huntingtin protein in AD and control CSF to determine the contribution of neurodegerenation to CSF HTT
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Investigator: Stephanie Vos
Project Title: Mechanisms of Neuronal Injury Subtypes in Early Alzheimer’s Disease
Date: [208]
Request ID: T1809 Vos
Aim 1: Overall aim: to understand the underlying mechanisms of different types of neuronal injury in early AD
Aim 2: Objective: to uncover the genetic and molecular mechanisms of cognitively normal individuals and individuals with mild cognitive impairment (CDR 0.5) with amyloid pathology and different measures of neuronal injury
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Investigator: GYUNGAH JUN
Project Title: Genomic and Biological Studies of APOE e2 in Alzheimer�s Disease
Date: [208]
Request ID: T1808
Aim 1: Determine the effect of eQTLs for the ɛ2-interacting variants on AD-related traits.
Aim 2: Assess effects of DNA methylation QTLs (mQTL) of the ɛ2 interacting genes on AD-related traits.
Aim 3: Identify associations between functional signatures of APOE ɛ2-interacting genes and protein levels of PPP2CB and neuroinflammatory genes, and quantitative neuropathological phenotypes.
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