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Reasearch Areas
  • Cell biology of CNS injury and repair
  • Animal models of CNS injury
  • Spinal cord injury
  • Brain Injury

Michael Beattie

Professor, University of California, San Francisco

My research program has been a cooperative effort with Dr. Jacqueline Bresnahan for many years, and has focused on the development of animal models for studying the biological and functional sequelae of brain and spinal cord injury and repair. Over the years, our laboratory has contributed to understandings of how neurons and oligodendrocytes undergo cell death after injury, as well as how regeneration and repair of axons and glial cells occur. We have developed outcome measures that have been useful in characterizing recovery after injury, including the highly cited ‘BBB’ locomotor rating scale, and more recently, measures of forelimb function after cervical injuries in rodents and non-human primates.


Inoue T, Lin A, Ma X, McKenna SL, Creasey GH, Manley GT, Ferguson AR, Bresnahan JC, Beattie MS (2013) Combine SCI and TBI: Recovery of forelimb function after unilateral cervical spinal cord injury (SCI) is retarded by contralateral traumatic brain injury (TBI), and ipsilateral TBI balances the effects of SCI on paw placement. Exp. Neurol. 238: 136-147.

Ferguson AR, Irvine K-A, Gensel JC, Nielson JL, Lin A, Ly J, Segal MR, Bresnahan JC, Beattie MS (2013) Derivation of multivariate syndromic outcome metrics for consistent testing across multiple models of cervical spinal cord injury in rats. PLoS One, 8(3) e59712.

Beattie EC, Stellwagen D, Morishita W, Bresnahan J, Ha B-K, Von Zastrow M, Beattie MS*, Malenka RC* (2002) Control of synaptic strength by glial TNFalpha. Science, 295: 2282-2285. *co-corresponding

Sun F, Shan X, McTigue D, Lin C-L, Bresnahan JC, Beattie MS (2010) Axonal degeneration induces microglial activation and oligodendrocyte precursor proliferation after dorsal rhizotomy and spinal cord injury, while oligodendrocyte death is associated with central injury and oxidative stress. Glia, 58: 1304-1319. PMC: NIHMS#273504.

Ferguson AR, Christensen RN, Miller BA, Sun F, Beattie EC, Bresnahan JC, Beattie MS (2008). Cell death after spinal cord injury is exacerbated by rapid TNF-alpha-induced trafficking of GluR2-lacking AMPARs to the plasma membrane. J. Neurosci. 28(44):11391–11400. PMC2598739.

Beattie MS (2004) Inflammation and apoptosis: linked therapeutic targets for spinal cord injury. Trends in Molecular Medicine, 10: 580-583.