Tisch MSRCNY conducted the first-ever FDA-approved Phase II placebo-controlled, double-blind clinical trial to investigate the use of mesenchymal stem cell treatment for patients with progressive MS. Since 2004, our work in stem cells has led to significant progress in developing therapies for MS progression-related disability.

Tisch MSRCNY developed the first-ever animal model specificially for primary-progressive MS. This model provided robust evidence that PPMS is its own unique disease, distinct from other MS subtypes. We currently use the model to remove or mutate specific CSF components to dampen symptoms and slow disease progression, as well as test new PPMS therapies from partner organizations.

Why do some patients with relapsing-remitting MS go on to develop secondary-progressive MS, and others do not? We are culturing human primary cortical neurons with CSF from patients with both subtypes to measure the levels of degeneration that follow. We aim to identify which specific factors in seconday-progressive MS CSF are toxic, so that we can halt further progression of the disease.

Our team is engaged in a long-term effort to fully characterize the B-cell antibody response in MS to aid in finding a cure. To do this, we curate a library of patient-derived B-cells that are continuously tested to search for the immunodominant myelin protein and isolate the trigger agent of the disease.

Research suggests that the body's immune response to contracting Epstein-Barr virus (EBV) increases a person's likelihood of developing MS. Using a brain organoid model exposed to EBV, researchers are studying the mechanisms by which EBV contributes to MS. We are also investigating EBV-related immune activation markers in response to different treatments and stages of disease.

Our team produces cerebral organoids, or "mini brains", from patient-derived pluripotent stem cells that allow us to study disease progression in a highly controlled experimental system that mimics the structure of the brain. Current studies examine cell proliferative capacity, neuronal differentiation, white matter analysis, and the impact of environmental factors known to influence MS.