Contributions
Abstract: 191
Type: Oral
Major advances have been achieved in the treatment multiple sclerosis (MS), through the active development of immunotherapy. Acting on different cellular players of the immune system, these currently approved therapies reduce the relapse rate, with different efficiency and safety profiles. However, even if few drugs partially impact disability progression, prevention of disability accumulation, which mostly correlates to irreversible neuronal/axonal damage and loss, is still an unmet need in MS, notably during the progressive phase of the disease. Although different (and not exclusive) mechanisms might result in neuronal and axonal pathology, increased neuronal/axonal vulnerability related to chronic demyelination is likely playing a key role.
Several studies, on experimental models of MS on the one hand, on post-mortem MS tissue on the other hand, have demonstrated the neuroprotective role of remyelination. Promoting remyelination is therefore a promising therapeutic strategy to prevent disability accumulation in MS.
In this context, recent years have been fruitful in our understanding of the cellular and molecular mechanisms of the remyelination process, through a wide variety of demyelination/remyelination models. This has resulted in the identification of potential therapeutic targets for remyelination. In parallel, the development of complementary screening tools has lead to the identification of several therapeutic candidates. Finally clinical translation is emerging , with few early phases clinical trials in MS patients. Aside from these strategies aimed at promoting endogenous repair, favouring exogenous remyelination through grafts is a very busy field of research, with different pre-clinical strategies actively developing.
We will discuss these recent and promising advances, but also the potential obstacles of these remyelination strategies, among them the need of markers of neuroprotection (or damage) and remyelination (or persisting demyelination) to evaluate therapeutic efficacy.
Disclosure: Participation to advisory boards of : ROCHE, NOVARTIS, GENZYME, BIOGEN VERTEX
Abstract: 191
Type: Oral
Major advances have been achieved in the treatment multiple sclerosis (MS), through the active development of immunotherapy. Acting on different cellular players of the immune system, these currently approved therapies reduce the relapse rate, with different efficiency and safety profiles. However, even if few drugs partially impact disability progression, prevention of disability accumulation, which mostly correlates to irreversible neuronal/axonal damage and loss, is still an unmet need in MS, notably during the progressive phase of the disease. Although different (and not exclusive) mechanisms might result in neuronal and axonal pathology, increased neuronal/axonal vulnerability related to chronic demyelination is likely playing a key role.
Several studies, on experimental models of MS on the one hand, on post-mortem MS tissue on the other hand, have demonstrated the neuroprotective role of remyelination. Promoting remyelination is therefore a promising therapeutic strategy to prevent disability accumulation in MS.
In this context, recent years have been fruitful in our understanding of the cellular and molecular mechanisms of the remyelination process, through a wide variety of demyelination/remyelination models. This has resulted in the identification of potential therapeutic targets for remyelination. In parallel, the development of complementary screening tools has lead to the identification of several therapeutic candidates. Finally clinical translation is emerging , with few early phases clinical trials in MS patients. Aside from these strategies aimed at promoting endogenous repair, favouring exogenous remyelination through grafts is a very busy field of research, with different pre-clinical strategies actively developing.
We will discuss these recent and promising advances, but also the potential obstacles of these remyelination strategies, among them the need of markers of neuroprotection (or damage) and remyelination (or persisting demyelination) to evaluate therapeutic efficacy.
Disclosure: Participation to advisory boards of : ROCHE, NOVARTIS, GENZYME, BIOGEN VERTEX