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Articles by Virginia M.Y. Lee
Total Records ( 2 ) for Virginia M.Y. Lee
  Michal J. Figurski , Teresa Waligorska , Jon Toledo , Hugo Vanderstichele , Magdalena Korecka , Virginia M.Y. Lee , John Q. Trojanowski and Leslie M. Shaw
  Background The interassay variability and inconsistency of plasma β-amyloid (Aβ) measurements among centers are major factors precluding the interpretation of results and a substantial obstacle in the meta-analysis across studies of this biomarker. The goal of this investigation was to address these problems by improving the performance of the bioanalytical method. Methods We used the Luminex immunoassay platform with a multiplex microsphere-based reagent kit from Innogenetics. A robotic pipetting system was used to perform crucial steps of the procedure. The performance of this method was evaluated using two kit control samples and two quality control plasma samples from volunteer donors, and by retesting previously assayed patient samples in each run. This setup was applied to process 2454 patient plasma samples from the Alzheimer‘s Disease Neuroimaging Initiative study biofluid repository. We have additionally evaluated the correlations between our results and cerebrospinal fluid (CSF) biomarker data using mixed-effects modeling. Results The average precision values of the kit controls were 8.3% for Aβ1-40 and 4.0% for Aβ1-42, whereas the values for the plasma quality controls were 6.4% for Aβ1-40 and 4.8% for Aβ1-42. From the test–retest evaluation, the average precision was 7.2% for Aβ1-40 and 4.5% for Aβ1-42. The range of final plasma results for Alzheimer‘s Disease Neuroimaging Initiative patients was 13 to 372 pg/mL (median: 164 pg/mL) for Aβ1-40 and 3.5 to 103 pg/mL (median: 39.3 pg/mL) for Aβ1-42. We found that sample collection parameters (blood volume and time to freeze) have a small, but significant, influence on the result. No significant difference was found between plasma Aβ levels for patients with Alzheimer‘s disease and healthy control subjects. We have determined multiple significant correlations of plasma Aβ1-42 levels with CSF biomarkers. The relatively strongest, although modest, correlation was found between plasma Aβ1-42 levels and CSF p-tau181/Aβ1-42 ratio in patients with mild cognitive impairment. Plasma Aβ1-40 correlations with CSF biomarkers were weaker and diminished completely when we used longitudinal data. No significant correlations were found for the plasma Aβ1-42/Aβ1-40 ratio. Conclusions The precision of our robotized method represents a substantial improvement over results reported in the literature. Multiple significant correlations between plasma and CSF biomarkers were found. Although these correlations are not strong enough to support the use of plasma Aβ measurement as a diagnostic screening test, plasma Aβ1-42 levels are well suited for use as a pharmacodynamic marker.
  Mitchel A. Kling , John Q. Trojanowski , David A. Wolk , Virginia M.Y. Lee and Steven E. Arnold
  Vascular disease was once considered the principal cause of aging-related dementia. More recently, however, research emphasis has shifted to studies of progressive neurodegenerative disease processes, such as those giving rise to neuritic plaques, neurofibrillary tangles, and Lewy bodies. Although these studies have led to critical insights and potential therapeutic strategies, interest in the role of systemic and cerebrovascular disease mechanisms waned and has received relatively less attention and research support. Recent studies suggest that vascular disease mechanisms play an important role in the risk for aging-related cognitive decline and disorders. Vascular disease frequently coexists with cognitive decline in aging individuals, shares many risk factors with dementias considered to be of the ”Alzheimer type,“ and is observed more frequently than expected in postmortem material from individuals manifesting ”specific“ disease stigmata, such as abundant plaques and tangles. Considerable difficulties have emerged in attempting to classify dementias as being related to vascular versus neurodegenerative causes, and several systems of criteria have been used. Despite multiple attempts, a lack of consensus remains regarding the optimal means of incorporating vascular disease into clinical diagnostic, neurocognitive, or neuropathologic classification schemes for dementias. We propose here an integrative, rather than a strictly taxonomic, approach to the study and elucidation of how vascular disease mechanisms contribute to the development of dementias. We argue that, instead of discriminating between, for example, ”Alzheimer's disease,“ ”vascular dementia,“ and other diseases, there is a greater need to focus clinical and research efforts on elucidating specific pathophysiologic mechanisms that contribute to dementia phenotypes and neuropathologic outcomes. We outline a multitiered strategy, beginning with clinical and public health interventions that can be implemented immediately, enhancements to ongoing longitudinal studies to increase their informative value, and new initiatives to capitalize on recent advances in systems biology and network medicine. This strategy will require funding from multiple public and private sources to support collaborative and interdisciplinary research efforts to take full advantage of these opportunities and realize their societal benefits.
 
 
 
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