Research Topics
| BARBARA SNIDERSummaryAffiliation: Washington University School of Medicine Country: USA Publications
Research Grants
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Detail Information
Publications
Apoptosis and necrosis in cerebrovascular diseaseB J Snider
Center for the Study of Nervous System Injury, Washington University School of Medicine, St Louis, Missouri 63110, USA
Ann N Y Acad Sci 893:243-53. 1999..Neurons may undergo both apoptosis and necrosis after ischemic insults, and thus it may be therapeutically desirable to block both processes...- NMDA antagonists exacerbate neuronal death caused by proteasome inhibition in cultured cortical and striatal neuronsB Joy Snider
Center for the Study of Nervous System Injury and Department of Neurology, Washington University School of Medicine, St Louis, MO, USA
Eur J Neurosci 15:419-28. 2002..In particular, concern is raised that glutamate receptor antagonists might exacerbate, rather than attenuate, proteasome inhibition-induced neuronal death... - Neocortical neurons cultured from mice with expanded CAG repeats in the huntingtin gene: unaltered vulnerability to excitotoxins and other insultsB J Snider
Center for the Study of Nervous System Injury and Department of Neurology, Washington University School of Medicine, Campus Box 8111, 660 South Euclid, St Louis, MO 63110, USA
Neuroscience 120:617-25. 2003..These observations suggest that expression of expanded polyglutamine-containing huntingtin does not acutely alter the vulnerability of cortical neurons to excitotoxic, oxidative or apoptotic insults... 
Cerebrospinal fluid biomarkers and rate of cognitive decline in very mild dementia of the Alzheimer typeBarbara J Snider
Department of Neurology, Washington University School of Medicine, Campus Box 8111, 660 S Euclid, St Louis, MO 63110, USA
Arch Neurol 66:638-45. 2009..Cerebrospinal fluid (CSF) levels of Abeta peptide 1-42 (Abeta 42), tau, and phosphorylated tau (ptau) are potential biomarkers of Alzheimer disease...- Novel presenilin 1 mutation (S170F) causing Alzheimer disease with Lewy bodies in the third decade of lifeB Joy Snider
Alzheimer s Disease Research Center, Washington University School of Medicine, St Louis, MO, USA
Arch Neurol 62:1821-30. 2005..We describe herein a kindred with very early-onset FAD (age, <40 years) with unusual pathological features and a novel mutation in the presenilin 1 (PSEN1) gene (S170F) and review the existing literature on very early-onset FAD... - Cellular calcium deficiency plays a role in neuronal death caused by proteasome inhibitorsShengzhou Wu
Laboratory of B Joy Snider, Hope Center for Neurological Disorders, Saint Louis, Missouri 63110, USA
J Neurochem 109:1225-36. 2009..These findings may have implications for the treatment of disorders associated with protein misfolding in which proteasome impairment and programmed cell death may occur... - Transient encephalopathy in a postoperative non-alcoholic female with Marchiafava-Bignami diseaseLesli E Rusche-Skolarus
Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
Clin Neurol Neurosurg 109:713-5. 2007..She returned to baseline after vitamin supplementation. We believe it is important to diagnose MBD because it is a potentially reversible encephalopathy... - Optimal promoter usage for lentiviral vector-mediated transduction of cultured central nervous system cellsMingjie Li
Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
J Neurosci Methods 189:56-64. 2010..These findings may prove useful in the design of lentiviral vectors for use in cell culture models of the nervous system... - A proteasomal stress response: pre-treatment with proteasome inhibitors increases proteasome activity and reduces neuronal vulnerability to oxidative injuryChul-Sang Lee
Center for the Study of Nervous System Injury and Department of Neurology, Washington University School of Medicine, St. Louis, Missouri 63110, USA
J Neurochem 91:996-1006. 2004.... - Raising intracellular calcium attenuates neuronal apoptosis triggered by staurosporine or oxygen-glucose deprivation in the presence of glutamate receptor blockadeLorella M T Canzoniero
Center for the Study of Nervous System Injury and Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, USA
Neurobiol Dis 15:520-8. 2004..Raising [Ca(2+)](i) either by activating voltage-sensitive Ca(2+) channels with (-) Bay K8644 or by application of low concentrations of kainate attenuated both staurosporine and oxygen-glucose deprivation-induced apoptosis... - Potassium channel blockers attenuate hypoxia- and ischemia-induced neuronal death in vitro and in vivoLing Wei
Center for the Study of Nervous System Injury and Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
Stroke 34:1281-6. 2003.... - A role for the ubiquitin-proteasome system in activity-dependent presynaptic silencingXiaoping Jiang
Department of Psychiatry, Washington University School of Medicine, St Louis, Missouri 63110, USA
J Neurosci 30:1798-809. 2010..These results suggest that modulation of the UPS by electrical activity contributes to persistent presynaptic silencing by promoting the degradation of key presynaptic proteins... - Lentiviral transduction of murine oligodendrocytes in vivoSally R McIver
Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, Missouri 63110, USA
J Neurosci Res 82:397-403. 2005.... - Neurotrophin and GDNF family ligands promote survival and alter excitotoxic vulnerability of neurons derived from murine embryonic stem cellsChul Sang Lee
Washington University School of Medicine, Center for the Study of Nervous System Injury, St Louis, MO 63110, USA
Exp Neurol 191:65-76. 2005..These findings demonstrate that the response of ES-derived neurons to neurotrophins and GDNF family ligands is largely similar to that of other cultured central neurons...
Research Grants
- Neuroprotective Effects of Enhanced Proteasome FunctionBARBARA SNIDER; Fiscal Year: 2006....