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The Miami Project to Cure Paralysis is a unique research center for many reasons, but probably one of the most important reasons is the leveraging power made possible by all of the donors to The Buoniconti Fund to Cure Paralysis.

In today’s world of grant funding, the pool of applicants is increasing while the pot of available funds is remaining level or, in some cases, decreasing or disappearing altogether.  Hence, in order for grant applications to be competitive, preliminary data regarding the research questions being tested need to be included to show the likelihood of success if funded.  However, that creates a situation similar to “having the cart before the horse”.  How is one supposed to generate data without funds to conduct the experiments?  That is where philanthropy becomes critically important and The Buoniconti Fund to Cure Paralysis has been instrumental in making possible significant scientific advances in the field of spinal cord injury.  

All of the private funds that have been generously donated to The Miami Project via The Buoniconti Fund over the last 25 years have enabled our researchers to generate the crucial preliminary data necessary to be awarded larger grants to further enhance our understanding of trauma to the nervous system and work towards developing effective therapeutic interventions.  The ability to purchase supplies for experiments and support personnel to conduct the experiments, without fear of interruption between grants, is critical to the success of The Miami Project in carrying out its mission.

At this 25 year landmark, we’d like to highlight how this some of this seed money from many generous donors has been used to leverage additional, large sources of funding and has been critical to advancing the scientific understanding of spinal cord injury.



Using the power of genetic technology, Dr. John Bethea and his laboratory created mice that contained an inactive form of a gene that is very important in regulating inflammation and secondary tissue damage in the nervous system.  These mice are called transgenic, meaning they’ve had a change to their genetic makeup.  The gene that was inactivated is called nuclear factor ĸB (NF-ĸB) and it was only inactivated in astrocytes.  Astrocytes are a type of support cell found in the brain and spinal cord and after an injury they become strongly activated and actually end up causing additional tissue damage, i.e. secondary damage.  Dr. Bethea found that when mice that had NF-ĸB inactivated in astrocytes were subjected to a spinal cord injury, there was a reduced inflammatory response which led to less secondary damage and a smaller lesion size when compared to non-transgenic mice that were spinal cord injured.  As a result of those neuroprotective effects, there was significant improvement in locomotor function.  These mice have also been used to investigate the disease process underlying multiple sclerosis.  In a progressive model of multiple sclerosis, the absence of NF-ĸB in astrocytes reduces the disease severity and, thereby, limits the degree of functional loss.  The philanthropic investment in the generation of those transgenic mice has enabled Dr. Bethea to publish multiple research articles and to successfully compete in several grant opportunities.  He has been awarded 3 large National Institutes of Health (NIH) grants that last for 5 years each, 2 grants from the Craig H. Nielsen Foundation (CHNF), and 1 grant from the Department of Defense (DoD).  

Similarly, Dr. Dan Liebl generated a mutant mouse that is missing the gene for EphB3, a cellular signaling molecule that has been shown to be important in controlling many aspects of the developing and injured nervous system. With these mutant mice, Dr. Liebl discovered that EphB3 is important in the generation of new nerve cells from adult stem cells already present in the brain.  When EphB3 is missing, adult stem cells are capable of surviving better and expanding/self-renewing at a faster rate.  Slow self-renewal is one of the significant barriers to the utilization of adult stem cells as an autologous therapy for diseases requiring neural cell replacement, such as spinal cord injury and traumatic brain injury.  These mice were also instrumental in determining that Ephs are very important in regulating synaptic activity (i.e. communication) between individual nerve cells.  In the brain, this is critical for learning and memory.  In the spinal cord, this could be significant in the re-establishment of functional circuitry following injury.  The initial investment in these mice has resulted in multiple publications and 3 successful NIH grants awarded to Dr. Liebl.

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