The study's potential impact on acute spinal cord injury (SCI) treatment in humans is significant, offering a promising strategy to reduce secondary damage and functional loss. Currently lacking effective clinical treatments for SCI, this research could pave the way for innovative approaches. Additionally, the project contributes to advancing knowledge on the endogenous regulation of the neuroinflammatory response, crucial for developing therapeutic strategies. These insights not only hold promise for preventing neuronal damage progression but also offer opportunities for tissue regeneration. Beyond SCI, identifying common neuroinflammatory pathways may extend these benefits to neurodegenerative diseases like Alzheimer's and autoimmune diseases such as Multiple Sclerosis.
SCI is a major cause of death and disability in those under 40, peaking around 20 years. In the European Union, there were approximately 330,000 SCI patients in 2002, with around 13,000 new cases annually. The male-to-female ratio is about 4:1, and the mean age at injury varies across countries. The societal and individual costs of SCI-induced paralysis are substantial, with estimated lifetime costs per individual reaching $1 million in the USA. Annually, 4 billion euros are spent on SCI patient management and care, with potential higher costs in the expanded European Community. These figures exclude social costs and the challenges faced by affected individuals and their families. Adaptations like changing living quarters, vehicle modifications, and addressing everyday difficulties affect both the individual's life and society economically.
SCI has profound social consequences, impacting employment rates, with only 24% of quadriplegic and 34% of paraplegic patients employed eight years post-injury. Despite these challenges and the considerable socioeconomic burden, effective SCI treatment remains elusive. Recognizing the need for new recovery-promoting strategies, the European Assembly emphasizes the importance of intensified efforts in spinal cord injury research, highlighting prevention and financial support. In light of these factors, the study not only addresses a critical gap in SCI treatment but aligns with the broader call for comprehensive policies and advancements in disability research.
During this period, I had two publications in peer-review journals, one addressing the involvement of another immune receptor, CD200R1, in peripheral nerve regeneration, and the other addressing the role of CD300f in inflammaging (see publications). We are currently preparing a manuscript with the results obtained from this proposal and they will be part of the data necessary for applying to International Research Paraplegia (IRP) funding and for applying for funding calls from the Spanish government. Moreover, during this period I directed two master theses involving the role of CD300f in demyelination and a PhD thesis in the role of CD200R1. Finally, this fellowship allowed me a successful reintegration as I currently hold a Tenure lecture position at the host institution.
