Abstract
The use of non-selective tumor necrosis factor (TNF) inhibitors is well known in the
treatment of inflammatory diseases such as rheumatoid arthritis, Crohn’s disease, and psoriasis.
Its use in neurological disorders is limited however, due to rare adverse events of demyelination,
even in patients without preceding demyelinating disease. We review here the molecular and cellular
aspects of this neuroinflammatory process in light of a case of severe monophasic demyelination
caused by treatment with infliximab. Focusing on the role of TNF, we review the links between CNS
inflammation, demyelination, and neurodegenerative changes leading to permanent neurological
deficits in a young woman, and we discuss the growing evidence for selective soluble TNF inhibitors
as a new treatment approach in inflammatory and neurological diseases.
treatment of inflammatory diseases such as rheumatoid arthritis, Crohn’s disease, and psoriasis.
Its use in neurological disorders is limited however, due to rare adverse events of demyelination,
even in patients without preceding demyelinating disease. We review here the molecular and cellular
aspects of this neuroinflammatory process in light of a case of severe monophasic demyelination
caused by treatment with infliximab. Focusing on the role of TNF, we review the links between CNS
inflammation, demyelination, and neurodegenerative changes leading to permanent neurological
deficits in a young woman, and we discuss the growing evidence for selective soluble TNF inhibitors
as a new treatment approach in inflammatory and neurological diseases.
| Original language | English |
|---|---|
| Article number | 38 |
| Journal | Brain Sciences |
| Volume | 11 |
| Issue number | 1 |
| Number of pages | 7 |
| ISSN | 2076-3425 |
| DOIs | |
| Publication status | Published - 1. Jan 2021 |
Keywords
- Demyelination
- Infliximab
- TNF inhibitor