Mark Tuszynski 

Mark H. Tuszynski, MD, PhD 



Contact Information

Biomedical Research Facility II Room 2121 
La Jolla, CA

Phone: 858-534-8857
Fax: 858-534-5220

Mailing Address:
9500 Gilman Drive #0626
La Jolla, CA 92093-0626

Lab website

In his research program, Dr. Tuszynski seeks to gain a greater understanding of the role of neurotrophic factors in axonal growth and cell survival in the intact and injured adult central nervous system.

Dr. Tuszynski's research bridges basic mechanisms of neurobiological function and clinical translation. He initiated the first human trial of gene therapy for an adult neurodegenerative disorder — Alzheimer's disease (AD) — in April 2001. In that study, he delivered human nerve growth factor to the cholinergic basal forebrain to determine whether cholinergic cell loss can be reduced and cholinergic function amplified in people with AD.

Current Tuszynski Laboratory Research Topics: Biological Basis of Normal Learning and Memory Hypothesis: Growth factors modulate alterations in neuronal structure and function to physically represent experience in cortical neuronal systems.

This research program aims to identify neural mechanisms that lead to the representation of long-term experience (memory) in the brain. Learning in motor systems in the cortex is a key model in these studies.

Neurodegeneration, Aging, and AD Hypothesis: Neurons undergo functional decline in aging as a result of a combination of cell dysfunction and, in limited regions, cell death. Growth factors can ameliorate both cellular dysfunction and death in animal models of aging and degeneration, including AD.

This research is identifying mechanisms that underlie age-related loss of function in the nervous system. The therapeutic potential of gene delivery of growth factors is being explored as a possible treatment for age-related diseases such as AD and Parkinson's disease.

Spinal Cord Injury (SCI) Hypothesis: Combinatorial therapeutic strategies can enhance axonal plasticity and regeneration after acute and chronic SCI.

The failure of the spinal cord to regenerate after injury is caused by (1) lack of production of growth-promoting substances such as growth factors in the injury site, (2) lack of permissive bridges for axon growth within injury sites, (3) deficiency of strong signals for the injured cell to re-enter an active growth state, and (4) blockade of growth by inhibitors in the injured region.

This research program tests the ability of cells and growth factors to promote regeneration after SCI. Tested cells include stem cells, autologous bone marrow cells, Schwann cells, and fibroblasts. The Tuszynski group is examining both acute and chronic models of SCI.

Curriculum Vitae

Year Award
1975 Presidential Scholar, University of Minnesota
1977 Tau Beta Pi Honorary Society
1980 Wasie Foundation Scholar
1995 Silvio O. Conte Research Award, American Academy of Neurology
1998 Elected to American Neurological Association
1998 Fellow, American Society for Neural Transplantation and Repair
2000 Sanberg Memorial Award for Brain Repair
2001 Ariens Kappers Medal, Netherlands Institute for Brain Research
2001 National Paralysis Foundation, Spinal Cord Injury Research Award
2002 Barbara Haugh Alzheimer's Disease Research Award
2004 Visionary Award, Glenner Alzheimer's Association of San Diego
2008 Heiner Sell Memorial Lectureship, American Spinal Injury Association
2008 Ted Bullock Award, UCSD Neuroscience Program
2008 Adelson Award, American Society for Neurorehabilitation
2011 Goldberg Award Lecture, University of Rochester
2012 Zenith Award, Alzheimer's Association
2012 Elected to The Dana Alliance for Brain Initiatives
2013 Elected Fellow, American Neurological Association
2013 Jacoby Award, American Neurological Association
2015 Reeve-Irvine Medal

Weidner N, Ner A, Salimi N, Tuszynski MH. Spontaneous corticospinal axonal plasticity and functional recovery after adult CNS injury. Proc Nat Acad Sci, 2001; 98:3513-3518.

Conner JM, Culberson A, Packowski C, Chiba A, Tuszynski MH. Lesions of the basal forebrain cholinergic system impair task acquisition and abolish cortical plasticity associated with motor skill learning. Neuron, 2003, 38:819-829

Conner JM, Chiba AA, Tuszynski MH. The basal forebrain cholinergic system is essential for cortical plasticity and functional recovery following brain injury. Neuron, 2005, 46:173-9. 

Tuszynski MH et al.  A phase I clinical trial of nerve growth factor gene therapy for Alzheimer’s disease. Nature Medicine, 2005, 11:551-5. 

Tuszynski MH.  Challenges to the report of nogo antibody effects in primates.  Nature Medicine 2006; 12:1231-1232.

Ramanathan D, Conner JM, Tuszynski, MH. A form of motor cortical plasticity that correlates with recovery of function after brain injury. Proc Nat Acad Sci, 2006;10330:11370-11375.

Blesch A, Tuszynski MH. Spinal cord injury: Plasticity, regeneration and the challenge of translational drug development. Trends in Neurosciences. 2009; 32:41-47. PMID: 18977039

Nagahara A, Merrill DA, Coppola G, Tsukada S, Schroder BE, Shaked GM, Wang L, Blesch A, Kim A, Conner JC, Rockenstein E, Chao MV, Koo E, Geschwind D, Masliah, Chiba AA, Tuszynski MH. Neuroprotective effects of BDNF in rodent and primate models of Alzheimer’s disease. Nature Medicine, 2009, 15:331-337. PMCID: PMC2838375. 

Hollis ER, Jamshidi P, Low K, Blesch A, Tuszynski MH.  Induction of corticospinal regeneration by lentiviral trkB-Induced Erk activation, Proc Nat Acad Sci, 2009, 106:7215-7220. PMCID 2678459.

Kadoya K, Tsukada S, Lu P, Coppola G, Geschwind D, Flibin M, Blesch A, Tuszynski MH. Combined intrinsic and extrinsic neuronal mechanisms facilitate bridging axonal regeneration one year after spinal cord injury. Neuron, 2009; 29:165-172. PMCID 2773653.

Alto L, Havton LA, Conner JM, Hollis ER, Blesch A, Tuszynski MH. Chemotropic guidance facilitates axonal regeneration into brainstem targets and synapse formation after spinal cord injury. Nature Neuroscience, 2009, 12: 1106-1113. PMCID 2753201.

Tuszynski MH. Community corner: Mutant mice challenged as models of injury in the central nervous system. Nature Medicine, 2010, 16:860.

Rosenzweig ES, Courtine G, Jindrich DL, Brock JH, Ferguson AR, Strand SC, Nout YS, Roy RR, Miller DM, Beattie MS, Havton LA, Bresnahan JC, Edgerton VR, Tuszynski M. Extensive spontaneous plasticity of corticospinal projections after primate spinal cord injury. 
   Nature Neuroscience, 2010, 13:1505-1510.

Nagahara A, Tuszynski MH. Potential therapeutic uses of BDNF in neurological and psychiatric disorders. Nature Rev Drug Discov, 2011, 10:209-219.

Wang L, Conner JM, Rickert JL, Tuszynski MH. Structural plasticity within highly specific neuronal populations identifies a parcellation of motor learning. Proc Nat Acad Sci, 2011, 108:2545-2550. PMCID: PMC3038698.

Tuszynski MH and Steward O. Concepts and Methods for the Study of Axonal Regeneration in the CNS. Neuron, 2012; 74:777-91. PMCID: PMC3387806.

Yoon SO, Park DJ, Ryu JC, Ozer HG, Tep C, Shin YJ, Lim TH, Pastorino L, Kunwar AJ, Walton JC, Nagahara AH, Lu KP, Nelson RJ, Tuszynski MH, Huang K. JNK3 perpetuates metabolic stress induced by Aβ peptides. Neuron  2012; 75:824-37.

Lu P, Wang Y, Graham L, McHale K, Gao M, Wu D, Brock J, Blesch A, Rosenzweig ES, Havton LA, Zheng B, Conner JM, Marsala M, Tuszynski MH. Long-distance growth and connectivity of neural stem cells after severe spinal cord injury: Cell-intrinsic mechanisms overcome spinal inhibition. Cell  2012, 14;150:1264-73. PMCID: PMC3445432.

Lu P, Woodruff G, Wang Y, Graham L, Hunt M, Wu D, Boehle E, Ahmad R, Poplawski G, Brock J, Goldstein LSB, Tuszynski MH. Long-distance axonal growth from human induced pluripotent stem cells after spinal cord injury. Neuron, 2014; 83:789-96.

Friedli L, Rosenzweig ES, Barraud Q, Schubert M, Dominici M, Awai L, Nielson JL, Musienko P, Nout-Lomas Y, Zhong H, Zdunowski S, Roy RR, Strand SC, van den Brand R, EMSCI Study Group, Havton LA, Beattie MS, Bresnahan JC, Bézard E,, Bloch J, Edgerton VR, Ferguson AR, Curt A, Tuszynski MH, Courtine G. Pronounced species divergence in functional recovery after lateralized spinal cord injury: corticospinal tract properties favor primates. Science Translational Medicine  2015; 7:302.

Tuszynski MH, Yang JH, Barba D, U HS, Bakay R, Pay MM, Masliah E, Conner JM, Kobalka P, Roy S, Nagahara AH. Neuronal responses to nerve growth factor gene therapy in Alzheimer’s disease.  JAMA Neurology  2015; in press.

Biane JS, Takashima Y, Conner JM, Massimo Scanziani, Tuszynski MH. Thalamocortical projections exhibit plasticity onto behaviorally-relevant neurons during adult motor learning. Neuron 2016, in press.

Kadoya K, Paul Lu P,  Nguyen K, Lee-Kubli C, Yao L, Poplawski G, Dulin J, Takashima Y, Biane J, Conner J, Zhang S-C, Tuszynski MH. Robust corticospinal regeneration enabled by spinal cord reconstitution with homologous neural grafts. Nature Medicine, in press.