Vitaliy Ovod

Vitaliy Ovod
Washington University in St. Louis | WUSTL , Wash U · Department of Neurology

MS

About

33
Publications
5,563
Reads
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3,452
Citations
Citations since 2017
22 Research Items
2528 Citations
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20172018201920202021202220230100200300400500
20172018201920202021202220230100200300400500
Additional affiliations
July 2018 - present
Washington University in St. Louis
Position
  • Analyst
Description
  • Bateman Lab
November 2008 - June 2018
Washington University in St. Louis
Position
  • Analyst
November 2008 - November 2010
Washington University in St. Louis
Position
  • Software Engineer

Publications

Publications (33)
Article
Full-text available
Cerebrospinal fluid (CSF) amyloid-β peptide (Aβ)42/Aβ40 and the concentration of tau phosphorylated at site 181 (p-tau181) are well-established biomarkers of Alzheimer’s disease (AD). The present study used mass spectrometry to measure concentrations of nine phosphorylated and five nonphosphorylated tau species and phosphorylation occupancies (perc...
Article
Objective: In Alzheimer's disease, hyperphosphorylated tau is associated with formation of insoluble paired helical filaments that aggregate as neurofibrillary tau tangles and are associated with neuronal loss and cognitive symptoms. Dual orexin receptor antagonists decrease soluble amyloid-β levels and amyloid plaques in mouse models over-express...
Article
Full-text available
Introduction: Continuous measures of amyloid burden as measured by positron emission tomography (PET) are being used increasingly to stage Alzheimer's disease (AD). This study examined whether cerebrospinal fluid (CSF) and plasma amyloid beta (Aβ)42/Aβ40 could predict continuous values for amyloid PET. Methods: CSF Aβ42 and Aβ40 were measured wi...
Article
Introduction: Sleep deprivation increases cerebrospinal fluid (CSF) amyloid beta (Aβ) and tau levels; however, sleep's effect on Aβ and tau in plasma is unknown. Methods: In a cross-over design, CSF Aβ and tau concentrations were measured in five cognitively normal individuals who had blood and CSF collected every 2 hours for 36 hours during sle...
Article
Full-text available
The extracellular buildup of amyloid beta (Aβ) plaques in the brain is a hallmark of Alzheimer’s disease (AD). Detection of Aβ pathology is essential for AD diagnosis and for identifying and recruiting research participants for clinical trials evaluating disease-modifying therapies. Currently, AD diagnoses are usually made by clinical assessments,...
Article
Hyperphosphorylated tau isoforms (p‐tau) in cerebrospinal fluid (CSF) and plasma represent promising measures to monitor Alzheimer disease (AD) pathological changes. Brain amyloid deposition precedes tau aggregation and associated clinical decline by two decades. Several CSF and plasma p‐tau isoforms have been described as potential surrogates for...
Preprint
Full-text available
CSF Aβ42/Aβ40 and tau phosphorylated at site 181 (p-tau181) are well-established biomarkers of Alzheimer disease (AD). This study used mass spectrometry to measure concentrations of 9 phosphorylated and 5 non-phosphorylated species, and phosphorylation occupancies (phosphorylated/non-phosphorylated [%]) at 10 sites. In 750 individuals with a median...
Article
Objective To determine the diagnostic accuracy of a plasma Aβ42/Aβ40 assay in classifying amyloid PET status across global research studies using samples collected by multiple centers that utilize different blood collection and processing protocols. Methods Plasma samples (n=465) were obtained from three large Alzheimer’s Disease (AD) research coh...
Article
Recent advances in the development of novel Alzheimer’s disease (AD) measures of amyloid, tau, and neurodegeneration in cerebrospinal fluid (CSF) and blood have enabled a better understanding of the links between amyloid‐beta (Aβ), tau species and neurodegeneration in the brain, CSF, and blood. The discoveries of novel tau species in CSF and blood,...
Article
Full-text available
Introduction: Blood-based assays to measure brain amyloid beta (Aβ) deposition are an attractive alternative to the cerebrospinal fluid (CSF)-based assays currently used in clinical settings. In this study, we examined different blood-based assays to measure Aβ and how they compare among centers and assays. Methods: Aliquots from 81 plasma sampl...
Article
Full-text available
Importance Blood-based tests for brain amyloid-β (Aβ) pathology are needed for widespread implementation of Alzheimer disease (AD) biomarkers in clinical care and to facilitate patient screening and monitoring of treatment responses in clinical trials. Objective To compare the performance of plasma Aβ42/40 measured using 8 different Aβ assays when...
Article
Full-text available
In vivo gold standard for the ante-mortem assessment of brain β-amyloid pathology is currently β-amyloid PET or cerebrospinal fluid measures of β-amyloid42 or the β-amyloid42/β-amyloid40 ratio. The widespread acceptance of a biomarker classification scheme for the Alzheimer’s disease continuum has ignited interest in more affordable and accessible...
Article
Recent advances in understanding the links between amyloid‐beta (Aβ) and specific tau isoforms in brain, cerebrospinal fluid (CSF), and blood indicate that a cascade of events of Alzheimer’s disease (AD) pathophysiology begin with detection of altered CSF and blood Aβ 42/40 ratio, followed by increases in amyloid plaques by Positron Emission Tomogr...
Article
Background: Concentrations of soluble amyloid-β (Aβ) oscillate with the sleep-wake cycle in the interstitial fluid of mice and cerebrospinal fluid (CSF) of humans. Further, the concentration of Aβ in CSF increases during sleep deprivation. Stress and disruption of the circadian clock are additional mechanisms hypothesized to increase CSF Aβ levels...
Article
Objective: We examined whether plasma β-amyloid (Aβ)42/Aβ40, as measured by a high-precision assay, accurately diagnosed brain amyloidosis using amyloid PET or CSF p-tau181/Aβ42 as reference standards. Methods: Using an immunoprecipitation and liquid chromatography-mass spectrometry assay, we measured Aβ42/Aβ40 in plasma and CSF samples from 158...
Article
Sleep disturbances are associated with future risk of Alzheimer's disease. Disrupted sleep increases soluble amyloid-β, suggesting a mechanism for sleep disturbances to increase Alzheimer's disease risk. We tested this response in humans using indwelling lumbar catheters to serially sample cerebrospinal fluid while participants were sleep-deprived,...
Article
Full-text available
Introduction Cerebrospinal fluid analysis and other measurements of amyloidosis, such as amyloid-binding positron emission tomography studies, are limited by cost and availability. There is a need for a more practical amyloid β (Aβ) biomarker for central nervous system amyloid deposition. Methods We adapted our previously reported stable isotope l...
Article
Full-text available
Importance: Recent studies found that the concentration of amyloid-β (Aβ) fluctuates with the sleep-wake cycle. Although the amplitude of this day/night pattern attenuates with age and amyloid deposition, to our knowledge, the association of Aβ kinetics (ie, production, turnover, and clearance) with this oscillation has not been studied. Objectiv...
Article
Full-text available
The risk of Alzheimers Disease (AD) is highly dependent on apolipoprotein-E (ApoE) genotype. The reasons for ApoE isoform-selective risk are uncertain, however, both the amounts and structure of human ApoE isoforms have been hypothesized to lead to amyloidosis increasing risk for AD. In order to address the hypothesis that amounts of ApoE isoforms...
Article
Full-text available
Age is the single greatest risk factor for Alzheimer's disease with the incidence doubling every 5 years after age 65. However, our understanding of the mechanistic relationship between increasing age and the risk for Alzheimer's disease is currently limited. We therefore sought to determine the relationship between age, amyloidosis, and amyloid-be...
Article
Full-text available
Objective: The aim of this study was to measure the flux of amyloid-β (Aβ) across the human cerebral capillary bed in order to determine if transport into the blood is a significant mechanism of clearance for Aβ produced in the central nervous system (CNS).Methods: Time-matched blood samples were simultaneously collected from a cerebral vein (inclu...
Article
Full-text available
BACE, a β-secretase, is an attractive potential disease-modifying therapeutic strategy for Alzheimer's disease (AD) as it results directly in the decrease of amyloid precursor protein (APP) processing through the β-secretase pathway and a lowering of CNS amyloid-β (Aβ) levels. The interaction of the β-secretase and α-secretase pathway-mediated proc...
Article
Full-text available
The amyloid-β (Aβ) protein is diurnally regulated in both the cerebrospinal fluid and blood in healthy adults; circadian amplitudes decrease with aging and the presence of cerebral Aβ deposits. The cause of the Aβ diurnal pattern is poorly understood. One hypothesis is that the Amyloid Precursor Protein (APP) is diurnally regulated, leading to APP...
Article
Full-text available
Background Inhibition of Beta-site APP-cleaving enzyme 1 (BACE1), the β-secretase in the central nervous system (CNS), is an attractive potential disease modifying therapeutic strategy for Alzheimer's disease (AD) as it decreases amyloid precursor protein (APP) processing through the amyloidogenic pathway and CNS β-amyloid peptide levels. The inter...
Article
Full-text available
Alzheimer's disease (AD) is hypothesized to be caused by an overproduction or reduced clearance of amyloid-β (Aβ) peptide. Autosomal dominant AD (ADAD) caused by mutations in the presenilin (PSEN) gene have been postulated to result from increased production of Aβ42 compared to Aβ40 in the central nervous system (CNS). This has been demonstrated in...
Article
Full-text available
Conformational changes in adsorbed fibrinogen may enhance the exposure of platelet adhesive sites that are inaccessible in solution. To test this hypothesis, mass spectrometric methods were developed to quantify chemical modification of lysine residues following adsorption of fibrinogen to biomaterials. The quantitative method used an internal stan...
Article
Full-text available
Alzheimer’s disease is hypothesized to be caused by an imbalance between β-amyloid (Aβ) production and clearance that leads to Aβ accumulation in the central nervous system (CNS). Aβ production and clearance are key targets in the development of disease-modifying therapeutic agents for Alzheimer’s disease. However, there has not been direct evidenc...

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Projects

Project (1)
Project
To determine blood Aβ isoform level relationships to current and future levels of CSF Aβ and amyloid PET, using blood samples from cross-sectional and longitudinal studies of cognitively normal, AD, and other neurodegenerative dementias.