Joy Snider, MD, PhD

Professor of Neurology

Phone314-747-2107

Fax314-362-9462

Emailsniderj@neuro.wustl.edu

Board Certifications

  • Neurology - Certified

Related Links

Recognition

  • Recognized as one of the Top 44 Providers with the Highest Patient Satisfaction, Washington University School of Medicine, 2009, 2010

Publications

  • Moulder KL, Snider BJ, Mills SL, Buckles VD, Santacruz AM, Bateman RJ, Morris JC. Dominantly Inherited Alzheimer Network: facilitating research and clinical trials. Alzheimers Res Ther. 2013 Oct 17;5(5):48. [Epub ahead of print]
  • Snider BJ, Buckles VD. “Will I get Alzheimer disease?” when cognitively normal patients ask to be tested for Alzheimer disease. Continuum (Minneap Minn). 2013 Apr;19(2 Dementia):470-4.
  • Li M, Husic N, Lin Y, Snider BJ. Production of lentiviral vectors for transducing cells from the central nervous system. J Vis Exp. 2012 May 24;(63):e4031.
  • Li M, Husic N, Lin Y, Christensen H, Malik I, McIver S, LaPash Daniels CM, Harris DA, Kotzbauer PT, Goldberg MP, Snider BJ. Optimal promoter usage for lentiviral vector-mediated transduction of cultured central nervous system cells. J Neurosci Methods. 2010 May 30;189(1):56-64.
  • Jiang X, Litkowski PE, Taylor AA, Lin Y, Snider BJ, Moulder KL. A role for the ubiquitin-proteasome system in activity-dependent presynaptic silencing. J Neurosci. 2010 Feb 3;30(5):1798-809.
  • Snider BJ. Translational biomarkers for accelerating drug development: From preclinical to clinical – AAPS Workshop. IDrugs. 2009 Jul;12(7):428-31. No abstract available.
  • Snider BJ, Fagan AM, Roe C, Shah AR, Grant EA, Xiong C, Morris JC, Holtzman DM. Cerebrospinal fluid biomarkers and rate of cognitive decline in very mild dementia of the Alzheimer type. Arch Neurol. 2009 May;66(5):638-45.
  • Rusche-Skolarus LE, Lucey BP, Vo KD, Snider BJ. Transient encephalopathy in a postoperative non-alcoholic female with Marchiafava-Bignami disease. Clin Neurol Neurosurg. 2007 Oct;109(8):713-5. Epub 2007 Jun 21.
  • Snider BJ, Norton J, Coats MA, Chakraverty S, Hou CE, Jervis R, Lendon CL, Goate AM, McKeel DW Jr, Morris JC. Novel presenilin 1 mutation (S170F) causing Alzheimer disease with Lewy bodies in the third decade of life. Arch Neurol. 2005 Dec;62(12):1821-30.
  • McIver SR, Lee CS, Lee JM, Green SH, Sands MS, Snider BJ, Goldberg MP. Lentiviral transduction of murine oligodendrocytes in vivo. J Neurosci Res. 2005 Nov 1;82(3):397-403.
  • Wei L, Cui L, Snider BJ, Rivkin M, Yu SS, Lee CS, Adams LD, Gottlieb DI, Johnson EM Jr, Yu SP, Choi DW. Transplantation of embryonic stem cells overexpressing Bcl-2 promotes functional recovery after transient cerebral ischemia. Neurobiol Dis. 2005 Jun-Jul;19(1-2):183-93.
  • Lee CS, Tee LY, Dusenbery S, Takata T, Golden JP, Pierchala BA, Gottlieb DI, Johnson EM Jr, Choi DW, Snider BJ. Neurotrophin and GDNF family ligands promote survival and alter excitotoxic vulnerability of neurons derived from murine embryonic stem cells. Exp Neurol. 2005 Jan;191(1):65-76.
  • Canzoniero LM, Babcock DJ, Gottron FJ, Grabb MC, Manzerra P, Snider BJ, Choi DW. Raising intracellular calcium attenuates neuronal apoptosis triggered by staurosporine or oxygen-glucose deprivation in the presence of glutamate receptor blockade. Neurobiol Dis. 2004 Apr;15(3):520-8.
  • Qu Y, Vadivelu S, Choi L, Liu S, Lu A, Lewis B, Girgis R, Lee CS, Snider BJ, Gottlieb DI, McDonald JW. Neurons derived from embryonic stem (ES) cells resemble normal neurons in their vulnerability to excitotoxic death. Exp Neurol. 2003 Nov;184(1):326-36.

My laboratory is interested in exploring how neurons die in neurodegenerative disorders and stroke, with a specific focus on how abnormally folded proteins, such as amyloid b-peptide and polyglutamine-containing proteins, cause neuronal death. These proteins are involved in the pathogenesis of Alzheimer’s disease and several dominantly inherited neurologic diseases, such as Huntington’s disease, dentatopallidoluysian atrophy and several spinocerebellar ataxias. We initially focused on the ability of heat shock proteins or molecular chaperones to alter neuronal vulnerability to injury. More recently, we have examined the role of the proteasomal protein degradation system in neuronal injury. Most of our studies are done in primary neuronal cell culture, with an additional focus on neurons derived from murine embryonic stem cells.

Recently, we and others observed that neurons (and other cell types) can increase the function of the proteasomal protein degradation system in response to proteasome inhibition or oxidative stress. We are very interested in understanding how proteasome function is increased, and developing strategies to increase proteasome function as a potential therapeutic modality.

We are also interested in the mechanisms of neuronal death following proteasome inhibition or other injuries. Unlike neuronal death caused by over-stimulation of NMDA receptors (excitotoxic neuronal death), the neuronal death caused by inhibition of proteasome function is associated with a reduction, rather than an increase, in intracellular calcium levels ([Ca2+]i). If, as some studies suggest, proteasome function is impaired in the brains of patients with dementing disorders, these findings would suggest that treatments that reduce neuronal [Ca2+]i might exacerbate rather than reduce neuronal loss.