CSF constitutents as mediators of brain damage in demyelinating diseases of the central nervous system
Aperçu du projet
Most nerves in the brain are surrounded by myelin, an insulating cover that allows them communicate efficiently. Brain damage in multiple sclerosis (MS) results from two, partially independent processes. On one side there are recurring attacks of immune cells on the myelin, which are responsible for development of new symptoms that then typically improve to variable extent. On the other side, there is a gradual loss of neurons which causes progressive worsening of physical and mental symptoms. This second process is the major cause of disability in people with MS and not much is known about what causes it. The current treatments for MS modulate the immune system to prevent attacks, but do not have much effect on the gradual worsening of symptoms. Recent research has shown that lesions near the brain surface are common in people with progressive MS, and the loss of neurons is also worst near the surface. This pattern of damage suggests a process driven by some harmful factors diffusing into the brain from the fluid that surrounds it, called cerebrospinal fluid (CSF). It was thought that this pattern of injury at the brain surfaces only happened in MS, but more recently a similar pattern has been found in a newly recognized disease called myelin oligodendrocyte glycoprotein antibody associated disease (MOGAD). The goal of this research is to analyze the CSF in people with MS and MOGAD and look for substances in the CSF that are most concentrated in people who also have the strongest brain-surface damage, as measured through MRI. The overall objective of this project is to discover what causes the damage at the brain surface in both MS and MOGAD, develop tools to predict how well patients will do in the future, and provide new targets for developing therapies to stop disease progression.
Chef d'équipe
Giulia Fadda , Université d’Ottawa / University of Ottawa
Partenaire et Donateurs
Azrieli Foundation