Traumatic Brain Injury (TBI)/Ataxia

Traumatic brain injury (TBI) occurs when an external force injures the brain. Symptoms can include impairments in cognition, movement, social skills, emotions,
or behavior.

The major cause of TBI is trauma to the head which can occur by vehicle collision, falling, violence, etc.

Conventional treatment is largely supportive and includes physical therapy, speech therapy, occupational therapy, counseling, etc.

Many researchers are looking toward stem cell therapy to try and repair and regenerate the damaged brain tissue following TBI. Currently, the goal of stem cell treatment for TBI is to improve quality of life by increasing the electrical signal within the brain which can lead to improvements in cognition as well as muscle function, strength and tone
in the periphery.

If you would like to talk with an expert about your specific condition, please fill out the
form below:

  • Wish to explore treating this condition with us?

    Fill out the form below for free information

The most current research regarding stem cells and TBI is given below:

Cell therapies for traumatic brain injury
Matthew T. Harting, M.D., James E. Baumgartner, M.D., Laura L. Worth, M.D., Ph.D., Linda Ewing-Cobbs, Ph.D., Adrian P. Gee, Ph.D., Mary-Clare Day, R.N., B.S.N., and Charles S. Cox, Jr., M.D

Abstract: Preliminary discoveries of the efficacy of cell therapy are currently being translated to clinical trials. Whereas a significant amount of work has been focused on cell therapy applications for a wide array of diseases, including cardiac disease, bone disease, hepatic disease, and cancer, there continues to be extraordinary anticipation that stem cells will advance the current therapeutic regimen for acute neurological disease. Traumatic brain injury is a devastating event for which current therapies are limited. In this report the authors discuss the current status of using adult stem cells to treat traumatic brain injury, including the basic cell types and potential mechanisms of action, preclinical data, and the initiation of clinical trials.


Umbilical Cord-Derived Mesenchymal Stromal Cells Contribute to Neuroprotection in Neonatal Cortical Neurons Damaged by
Oxygen-Glucose Deprivation

Takeo Mukai, Arinobu Tojo, and Tokiko Nagamura-Inoue

Abstract: Several studies have reported that human umbilical cord-derived mesenchymal stromal cells (UC-MSCs) restore neurological damage in vivo through their secretion of paracrine factors. We previously found that UC-MSCs attenuate brain injury by secreting neurotrophic factors, such as brain-derived neurotrophic factor (BDNF) and hepatocyte growth factor (HGF). However, how these factors contribute to neuroprotection remains unknown. In this study, we aimed to investigate to what extent UC-MSC-derived HGF and BDNF contribute to neuroprotection using a Transwell co-culture system of neonatal cortical neurons damaged by oxygen-glucose deprivation. The influence of HGF and BDNF were determined by investigating neurons in both the presence and absence of UC-MSCs as these cells consistently secrete both factors and can be blocked by neutralizing antibodies. In the co-culture, UC-MSCs significantly improved neuronal injury, as indicated by an increase in immature neuron number, neurite outgrowth, and cell proliferation. Co-culture of damaged neurons with UC-MSCs also exhibited a reduction in the number of neurons displaying signs of apoptosis/necrosis. The neuroprotective actions of UC-MSCs were partially reverted by neutralizing antibodies. Together, our findings reveal that UC-MSC-secreted HGF and BDNF have neuroprotective effects on damaged neurons. Further studies should address the existence of other potential neurotrophic paracrine factors.