Houston Methodist. Leading Medicine.
Houston Methodist. Leading Medicine

David R. Beers, Ph.D.

David R. Beers, Ph.D.

 

David R. Beers, Ph.D.

David R. Beers, Ph.D.

Associate Research Member
The Methodist Hospital Research Institute

Assistant Professor, Department of Neurology
Director, Neurology Transgenic Animal Facility
The Methodist Neurological Institute

E-mail: dbeers@houstonmethodist.org
Phone: 713-441-3682
Fax: 713-441-3688


Education

B.S.   University of Utah, Salt Lake City, UT (Economics)
Ph.D.   University of Utah, Salt Lake City, UT (Neuroscience)

Postdoctoral Training

Fellowship, Department of Neurology, Baylor College of Medicine, Houston, TX
Fellowship, Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX
Fellowship, Department of Neurology, Baylor College of Medicine, Houston, TX

 

Biography

Dr. Beers received his first academic appointment in 1998 as an Instructor in the Department of Neurology at the Baylor College of Medicine. He would become an Assistant Professor there just two years later. In addition to authoring over 20 scientific papers, Dr. Beers is a co-investigator on a R01 grant from the NIH and a gene therapy study funded by the Muscular Dystrophy Association. His past research support also includes a NIH Pre-doctoral Individual National Research Service Award and a Postdoctoral Fellowship from the National Multiple Sclerosis Society. Dr. Beers assumed his positions at Methodist in 2005.

Description of Research

Dr. Beers’ research focuses on the mechanisms underlying neuronal injury and approaches to slowing the progression of neurodegeneration in preclinical models of amyotrophic lateral sclerosis (ALS). His current studies investigate the roles of innate and adaptive immune cells (microglia, T-cells, etc.) on disease initiation and progression.

Major Areas of Research

ALS, neurodegeneration, immune mechanisms, microglia

Recent Publications

Beers DR, Henkel JS, Zhao W, Wang J, and Appel SH. CD4+ T-Cells Support Glial Neuroprotection, Slow Disease Progression, and Modify Glial Morphology in an Animal Model of Inherited ALS. Proc Natl Acad Sci U S A. 2008;105(40):15558-63.

Appel, SH, Engelhardt, JI, Henkel, JS, Siklos, L, Beers, DR, Yen, AA, Simpson, EP, Luo, Y, Carrum, G, Heslop, HE, Brenner, MK, Popat, U. Hematopoietic Stem Cell Transplantation in Patients with Sporadic Amyotrophic Lateral Sclerosis. Neurology. 2008;71(17):1326-34.

Xiao Q, Zhao W, Beers DR, Yen AA, Xie W, Henkel JS, Appel SH. Mutant SOD1G93A microglia are more neurotoxic relative to wild-type microglia. J Neurochem. 2007;102(6):2008-2019.

Beers DR, Henkel JS, Xiao Q, Zhao W, Wang J, Yen AA, Siklos L, McKercher SR, Appel SH. Wild-type microglia extend survival in PU.1 knockout mice with familial amyotrophic lateral sclerosis. Proc Natl Acad Sci USA. 2006;103(43):16021-16026.

Zhao W, Xie W, Xiao Q, Beers DR, Appel SH. Protective effects of an anti-inflammatory cytokine, interleukin-4, on motoneuron toxicity induced by activated microglia. J Neurochem. 2006;99(4):1176-1187.

Henkel JS, Beers DR, Siklos L, Appel SH. The chemokine MCP-1 and the dendritic and myeloid cells it attracts are increased in the mSOD1 mouse model of ALS. Mol Cell Neurosci. 2006;31(3):427-437.

Zhao W, Xie W, Le W, Beers DR, He Y, Henkel JS, Simpson EP, Yen AA, Xiao Q, Appel SH. Activated microglia initiate motor neuron injury by a nitrite oxide and glutamate-mediated mechanism. J Neuropathol Exp Neurol. 2004;63(9):964-977.