Sophie Sokolow

ORCID: 0000-0002-9510-9062
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About
Contact & Profiles
Research Areas
  • Neuroscience and Neuropharmacology Research
  • Alzheimer's disease research and treatments
  • Ion channel regulation and function
  • Neuroscience and Neural Engineering
  • Cardiac electrophysiology and arrhythmias
  • Cholinesterase and Neurodegenerative Diseases
  • Memory and Neural Mechanisms
  • Neuroinflammation and Neurodegeneration Mechanisms
  • 14-3-3 protein interactions
  • Computational Drug Discovery Methods
  • Dementia and Cognitive Impairment Research
  • Pain Mechanisms and Treatments
  • Folate and B Vitamins Research
  • Calcium Carbonate Crystallization and Inhibition
  • Physiological and biochemical adaptations
  • Coenzyme Q10 studies and effects
  • Protein Tyrosine Phosphatases
  • Parkinson's Disease Mechanisms and Treatments
  • Biomedical and Chemical Research
  • Advanced Memory and Neural Computing
  • Musculoskeletal pain and rehabilitation
  • Exercise and Physiological Responses
  • bioluminescence and chemiluminescence research
  • ATP Synthase and ATPases Research
  • Cytokine Signaling Pathways and Interactions

University of California, Los Angeles
2009-2024

Université Libre de Bruxelles
2004-2022

UCLA Clinical and Translational Science Institute
2014-2016

Southern California Clinical and Translational Science Institute
2014-2016

University of Southern California
2015

Mayo Clinic in Arizona
2015

University of California, San Francisco
2015

VA Greater Los Angeles Healthcare System
2015

University of California, Berkeley
2015

University of Pennsylvania
2015

<h3>Abstract</h3> Cellular heterogeneity in the human brain obscures identification of robust cellular regulatory networks. Here we integrated genome-wide chromosome conformation purified neurons and glia with transcriptomic enhancer profiles to build gene landscape two major cell classes brain. Within glutamatergic GABAergic neurons, were able link enhancers their cognate genes via neuronal chromatin interaction profiles. These cell-type-specific landscapes then leveraged gain insight into...

10.1212/01.wnl.0000303973.71803.81 article EN Neurology 2008-05-29

Background Different cerebrospinal fluid (CSF) amyloid-beta 1–42 (A β ), total Tau (Tau) and phosphorylated at threonine 181 (P-Tau) levels are reported, but currently there is a lack of quality control programmes. The aim this study was to compare the measurements these CSF biomarkers, between within centres. Methods Three CSF-pool samples were distributed 13 laboratories in 2004 same again 18 2008. In six measured A , P-Tau seven one or two marker(s) by enzyme-linked immunosorbent assays...

10.1258/acb.2009.008232 article EN Annals of Clinical Biochemistry International Journal of Laboratory Medicine 2009-04-02

Abstract The microtubule‐associated protein tau has primarily been associated with axonal location and function; however, recent work shows release from neurons suggests an important role for in synaptic plasticity. In our study, we measured levels of total using synaptosomes prepared cryopreserved human postmortem Alzheimer's disease (AD) control samples. Flow cytometry data show that a majority terminals are highly immunolabeled the antibody (HT7) both AD Immunoblots synaptosomal fractions...

10.1111/jnc.12991 article EN Journal of Neurochemistry 2014-11-13

Na + /Ca 2+ exchanger 3 (NCX3), one of the three isoforms NCX family, is highly expressed in brain and involved maintenance intracellular Ca homeostasis. Interestingly, whereas function NCX3 under physiological conditions has been determined, its role anoxia still unknown. To assess cerebral ischemia, we exposed ncx3−/− mice to transient middle artery occlusion followed by reperfusion. In addition, evaluate effect ncx3 ablation on neuronal survival, organotypic hippocampal cultures primary...

10.1523/jneurosci.4671-07.2008 article EN cc-by-nc-sa Journal of Neuroscience 2008-01-30

Long-term potentiation (LTP) depends on the coordinated regulation of an ensemble proteins related to Ca 2+ homeostasis, including transporters. One major players in intracellular ([Ca ] i ) homeostasis neurons is sodium/calcium exchanger (NCX), which represents principal mechanism clearance synaptic sites hippocampal neurons. Because NCX3, one three brain isoforms NCX family, highly expressed subfields involved LTP, we hypothesized that it might represent a potential candidate for LTP...

10.1523/jneurosci.6296-10.2011 article EN cc-by-nc-sa Journal of Neuroscience 2011-05-18

The immune response to dystrophin-deficient muscle promotes the pathology of Duchenne muscular dystrophy (DMD) and mdx mouse model DMD. In this investigation, we find that release major basic protein (MBP) by eosinophils is a prominent feature DMD lyse cells in vitro MBP-1. We also show eosinophil depletions mice injections anti-chemokine receptor-3 reduce cell lysis, although lysis membranes not reduced null mutation MBP-1 vivo. However, ablation expression produces other effects on...

10.1093/hmg/ddn129 article EN Human Molecular Genetics 2008-04-17

Like amyloid beta (Aβ) oligomers, tau aggregates are increasingly recognized as potential key toxic intermediates in Alzheimer's disease (AD) and therapeutic targets. P-tau co-localizes with Aβ cortical AD synapses may contribute to synapse dysfunction loss. Flow cytometry analysis of synaptosomes from compared aged cognitively normal cortex demonstrates increased immunolabeling for three p-tau antibodies (AT8, PHF-1 pS422), indicating phosphorylation at multiple epitopes. Sequential...

10.1111/j.1750-3639.2012.00598.x article EN Brain Pathology 2012-04-10

We produced and analyzed mice deficient for Na/Ca exchanger 3 (NCX3), a protein that mediates cellular Ca2+ efflux (forward mode) or influx (reverse thus controls intracellular concentration. NCX3-deficient (Ncx3–/–) present skeletal muscle fiber necrosis defective neuromuscular transmission, reflecting the absence of NCX3 in sarcolemma fibers at junction. The transmission is characterized by presence electromyographic abnormalities, including low compound action potential amplitude,...

10.1172/jci18688 article EN Journal of Clinical Investigation 2004-01-15
Liana G. Apostolova Kristy Hwang David Ávila David Elashoff Omid Kohannim and 95 more Edmond Teng Sophie Sokolow Clifford R. Jack William J. Jagust Leslie M. Shaw John Q. Trojanowski Michael W. Weiner Paul M. Thompson Michael W. Weiner Paul Aisen Ronald Petersen Clifford R. Jack Wiliam Jagust John Q. Trojanowki Arthur W. Toga Laurel Beckett Robert C. Green Anthony Gamst Andrew J. Sakin John C. Morris William Z. Potter Tom Montine Michael Donohue Sarah Walter Anders M. Dale Matt A. Bernstein Joel P. Felmlee Nick C. Fox Paul M. Thompson Norbert Schuff Gene E. Alexander Charles DeCarli Dan Bandy Robert A. Koeppe Norm Foster Eric M. Reiman Kewei Chen Chester A. Mathis Nigel J. Cairns Lisa Taylor‐Reinwald Lee Shaw Virginia M.‐Y. Lee Magdalena Korecka Karen Crawford Scott Neu Danielle Harvey John Kornak Tatiana Foroud Steven G. Potkin Li Shen Zaven Kachaturian Richard Frank Peter J. Snyder Susan Molchan Jeffrey Kaye Sara Dolen Joseph F. Quinn Lon S. Schneider Sonia Pawluczyk Bryan M. Spann James B. Brewer Helen Vanderswag Judith L. Heidebrink Joanne Lord Kris Johnson Rachelle S. Doody Javier Villanueva‐Meyer Munir Chowdhury Yaakov Stern Lawrence S. Honig Karen L. Bell Mark A. Mintun Stacy Schneider Daniel Marson Randall Griffith David Clark Hillel Grossman Cheuk Y. Tang George Marzloff Leyla deToledo‐Morrell Raj C. Shah Ranjan Duara Daniel Varón Peggy Robers Marilyn S. Albert Nicholas Kozauer Maria Zerrate Henry Rusinek Mony J. de Leon Susan M De Santi P. Murali Doraiswamy Jeffrey R. Petrella Marilyn Aiello S. R. Arnold Jason Karlawish

<h3>Background:</h3> The goal of this study was to identify a clinical biomarker signature brain amyloidosis in the Alzheimer9s Disease Neuroimaging Initiative 1 (ADNI1) mild cognitive impairment (MCI) cohort. <h3>Methods:</h3> We developed multimodal classifier for predicting using cognitive, imaging, and peripheral blood protein ADNI1 MCI data. used CSF β-amyloid 1–42 (Aβ<sub>42</sub>) ≤192 pg/mL as proxy measure Pittsburgh compound B (PiB)-PET standard uptake value ratio ≥1.5. trained our...

10.1212/wnl.0000000000001231 article EN Neurology 2015-01-22

Donepezil is an acetylcholinesterase inhibitor frequently prescribed for the treatment of mild cognitive impairment (MCI) though not approved by Food and Drug Administration this indication. In Alzheimer's disease, butyrylcholinesterase (BChE) activity increases with disease progression may replace function. The most frequent polymorphism BChE K-variant, which associated lower acetylcholine-hydrolyzing activity. BChE-K has been studied in donepezil therapy, led to contradictory results. To...

10.3233/jad-160562 article EN Journal of Alzheimer s Disease 2016-11-29

The Na + /Ca 2+ exchanger NCX3, recently identified as a myelin membrane component, is involved in the regulation of [Ca ]i during oligodendrocyte maturation. Here NCX3 involvement was studied glycoprotein (MOG)‐induced experimental autoimmune encephalomyelitis (EAE), an animal model multiple sclerosis. Western blotting and quantitative colocalization studies performed wild‐type ncx3 +/+ mice at different stages EAE disease showed that protein intensely upregulated chronic stage, where it...

10.1002/glia.22985 article EN Glia 2016-04-27

Abstract Amyloid beta (Aβ) oligomers and phosphorylated tau (p‐tau) aggregates are increasingly identified as potential toxic intermediates in Alzheimer's disease (AD). In cortical AD synapses, p‐tau co‐localizes with Aβ, but the Aβ peptide species responsible for synaptic dysfunction demise remains unclear. The present experiments were designed to use high‐speed cell sorting techniques purify synaptosome population based on size, then extend method physically isolate Aβ‐positive...

10.1002/cyto.a.22009 article EN Cytometry Part A 2011-12-28

Repeated application of noxious stimuli leads to a progressively increased pain perception; this temporal summation is enhanced in and predictive clinical disorders. Its electrophysiological correlate "wind-up," which dorsal horn spinal neurons increase their response repeated nociceptor stimulation. To understand the genetic basis summation, we undertook GWAS wind-up healthy human volunteers found significant association with SLC8A3 encoding sodium-calcium exchanger type 3 (NCX3). NCX3 was...

10.1016/j.neuron.2022.05.017 article EN cc-by Neuron 2022-06-14

We have previously shown that overexpression of the Na-Ca exchanger (NCX1), a protein responsible for Ca(2+) extrusion from cells, increases β-cell programmed cell death (apoptosis) and reduces proliferation. To further characterize role NCX1 in β-cells under vivo conditions, we developed characterized mice deficient NCX1.Biologic morphologic methods (Ca(2+) imaging, uptake, glucose metabolism, insulin release, point counting morphometry) were used to assess function vitro. Blood levels...

10.2337/db10-0924 article EN cc-by-nc-nd Diabetes 2011-06-10

More than 500 unreclaimed mines and associated waste sites exist on the Navajo Nation reservation as a result of uranium (U) mining from 1940s through 1980s. For this study, impact U-mine common, locally grown crop food was examined. The goal site-specific study to determine metal(loid) concentration levels arsenic (As), cadmium (Cd), cesium (Cs), molybdenum (Mo), lead (Pb), thorium (Th), U, vanadium (V) selenium (Se) in Cucurbita pepo Linnaeus (squash), irrigation water, soil using...

10.3390/ijerph16142569 article EN International Journal of Environmental Research and Public Health 2019-07-18

Matrix vesicles (MVs) provide the initial site for amorphous hydroxyapatite (HA) formation within mineralizing osteoblasts. Although Na

10.1002/jev2.12450 article EN cc-by-nc-nd Journal of Extracellular Vesicles 2024-06-01

We produced and analyzed mice deficient for Na/Ca exchanger 3 (NCX3), a protein that mediates cellular Ca2+ efflux (forward mode) or influx (reverse thus controls intracellular concentration. NCX3-deficient (Ncx3–/–) present skeletal muscle fiber necrosis defective neuromuscular transmission, reflecting the absence of NCX3 in sarcolemma fibers at junction. The transmission is characterized by presence electromyographic abnormalities, including low compound action potential amplitude,...

10.1172/jci200418688 article EN Journal of Clinical Investigation 2004-01-15
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