Indeed, increased levels of TNF-α have been reported in cases of Alzheimer’s disease (AD), multiple sclerosis (MS) or rheumatoid arthritis (RA), among others 2, 3. However, alterations in the levels of TNF-α can be detrimental and have been related to several autoimmune and neurodegenerative diseases. TNF-α plays a key role in the initiation of the innate and adaptive immune system and its expression is thus tightly regulated 1. Tumor necrosis factor alpha (TNF-α) is a master pro-inflammatory cytokine secreted by activated immune cells upon infections or tissue damage. Altogether, our study indicates that Atrosimab may be a promising candidate for the development of a therapeutic strategy for the treatment of neurodegenerative diseases. Our results demonstrate that Atrosimab is effective in ameliorating disease symptoms in an acute neurodegenerative mouse model. We showed that Atrosimab attenuated cognitive impairments and reduced neuroinflammation and neuronal cell death. In this model, a NMDA-induced lesion that mimics various hallmarks of neurodegenerative diseases, such as memory loss and cell death, was created in the nucleus basalis magnocellularis and Atrosimab or control protein was administered centrally. Here, we investigated the effect of administering the TNFR1-specific antagonist Atrosimab, as strategy to block TNFR1 signaling while maintaining TNFR2 signaling unaltered, in an acute mouse model for neurodegeneration. TNF-α exerts distinct functions depending on interaction with its two TNF receptors, whereby TNF receptor 1 (TNFR1) is associated with neuroinflammation and apoptosis and TNF receptor 2 (TNFR2) with neuroprotection and immune regulation. Even though inhibition of TNF-α is beneficial for the treatment of certain inflammatory diseases, total neutralization of TNF-α largely failed in the treatment of neurodegenerative diseases. Tumor necrosis factor alpha (TNF-α) and its key role in modulating immune responses has been widely recognized as a therapeutic target for inflammatory and neurodegenerative diseases.
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |