Community Research and Development Information Service - CORDIS

FP6

NEUROPROMISE — Result In Brief

Project ID: 18637
Funded under: FP6-LIFESCIHEALTH
Country: Italy

Fathoming MS

An EU-funded project increased our knowledge about the processes involved in the pathology of multiple sclerosis. Improved understanding in this area stands to impact the development of rational treatment and therapies.
Fathoming MS
Multiple sclerosis (MS), the most common chronic inflammatory disease of the central nervous system, has been widely studied. However, the genetic basis of this neurological disability is still unknown and scientists are only beginning to understand the mechanisms underlying brain injury. There is no curative therapy available and no drugs have been able to halt the neurodegenerative process that drives disease progression.

The 'Neuroprotective strategies for multiple sclerosis' (Neuropromise) project investigated in depth the genetic and mechanistic pathways playing a role in inflammation-induced neurodegeneration. Bringing together expertise from a wide range of medical and scientific fields, the EU-funded project also aimed to exploit knowledge gained to drive development of improved therapeutic agents.

Results of the genetic studies carried out contributed greatly to a better understanding of how genes outside the major histocompatibility complex (MHC) locus contribute to disease development. Knowing more about the pathways that individual non-MHC genes are involved in thus opened the path to gaining new insights into the complex mechanisms underlying MS pathogenesis.

Given that axon injury and degeneration play a significant role in MS pathology, knowledge of the molecular mechanisms involved is critical for designing effective neuroprotective therapies. Researchers used transcriptomics and proteomics approaches to identify early molecular changes taking place in axonal projections of defined neuronal populations. They also examined whole brain tissue in different experimental models of neuroinflammation and neurodegeneration. The transcript and protein patterns identified were then subjected to extensive bioinformatic analysis, and validated with relevant techniques.

Project outcomes significantly advanced understanding of MS and neuroinflammatory processes overall. With the knowledge acquired, team members proposed more reliable models of MS pathogenesis and developed candidate therapeutic molecules for clinical evaluation.

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