The biological basis of progressive MS, both secondary (SPMS) and primary (PPMS) is poorly understood pathologically and is generally treatment unresponsive. It is a difficult problem to investigate because the widely used animal model of MS, experimental allergic encephalomyelitis (EAE) is not representative of progressive MS. Moreover, brain and spinal cord specimens from patients with progressive MS are not easily obtained and post-mortem lesion pathology does not represent the dynamic biological events pertaining to ongoing disease pathogenesis. In this scenario, investigation of cerebrospinal fluid (CSF) obtained from progressive MS is likely to yield important and new insights into the mechanisms of progressive disease.
The objective of Dr. Cristofanilli’s work is to establish in vitro and in vivo models of progressive MS to better understand mechanisms of disease progression, regeneration failure, and to screen for potential therapeutic agents. In Dr. Cristofanilli’s hypothesis, the agent(s) responsible for the loss of myelin and progressive neurodegeneration characteristic of progressive forms of MS is present in patients’ CSF and is capable of replicating the disease’s pathophysiological phenotype in cell culture and in mice.
Dr. Cristofanilli received his PhD in Neuroscience from University of Rome "La Sapienza", in a joint program with SUNYDown State Medical Center (NY). Prior to joining the Center, he was a research associate in the Keck Center for Collaborative Neuroscience at Rutgers University(NJ) from 2006-2008, and a postdoctoral fellow at NYU School of Medicine from 2005-2006 and at SUNY Down State Medical Center (NY) from 2003-2005.