Mark H. Tuszynski, MD, PhD 

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

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