Tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) in central nervous system inflammation

2009 ◽  
Vol 87 (8) ◽  
pp. 753-763 ◽  
Author(s):  
Olaf Hoffmann ◽  
Frauke Zipp ◽  
Joerg R. Weber
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Central Nervous System Inflammation ◽  
Necrosis Factor

Expression and Function of Tumour Necrosis Factor-α-Converting Enzyme in the Central Nervous System

Neurosignals ◽  
2003 ◽  
Vol 12 (2) ◽  
pp. 53-58 ◽  
Author(s):  
Maria A. Moro ◽  
Olivia Hurtado ◽  
Antonio Cárdenas ◽  
Cristina Romera ◽  
Jose L.M. Madrigal ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Converting Enzyme ◽  
Tumour Necrosis Factor Α ◽  
The Central Nervous System ◽  
Factor Α ◽  
And Function ◽  
Necrosis Factor

scholarly journals Central Nervous System Demyelination Related to Tumour Necrosis Factor Alpha Inhibitor

2022 ◽  
Vol 8 (1) ◽  
pp. 205521732110707
Author(s):  
Shin Yee Chey ◽  
Allan G. Kermode
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Tumour Necrosis ◽  
Tumour Necrosis Factor Alpha ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

Background An association between tumour necrosis factor alpha (TNF-α) inhibitors exposure and central nervous system (CNS) demyelinating disorders has been postulated but is poorly understood. Objectives Describe the clinical spectrum and progress of a cohort of patients who developed demyelinating disorder following exposure to TNF-α inhibitor. Methods Retrospective chart review of patients who presented to a single neurologist in Western Australia between May 2003 and July 2020. Results 7 patients (6 females and 1 male) were identified. Mean age was 49.1 years. Mean follow-up time was 2.9 years. Mean interval between commencement of TNF-α inhibitor and onset of demyelinating event was 3 years. The spectrum of demyelinating events included transverse myelitis ( N = 3), acute brainstem syndrome ( N = 1) and optic neuritis ( N = 1). 2 patients had an atypical presentation but had MRI findings which unequivocally showed demyelinating changes. 2 patients had a monophasic event while the other 5 patients were diagnosed to have multiple sclerosis. All symptomatic patients with multiple sclerosis were started on disease modifying therapy and remained relapse free during follow-up. Conclusion Exposure to TNF-α inhibitor appears to increase the risk of demyelinating event. Whether TNFα inhibition directly results in CNS demyelination or trigger demyelination in susceptible individuals requires further research.

scholarly journals VITAMIN B12 AND NORMAL PRIONS: TWO FIELDS APPARENTLY SO FAR, BUT IN REALITY SO NEAR

2014 ◽  
Author(s):  
Giuseppe Scalabrino ◽  
Daniela Veber
Keyword(s):  
Multiple Sclerosis ◽  
Spinal Cord ◽  
Nervous System ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Post Mortem ◽  
The Central Nervous System ◽  
Epidermal Growth ◽  
And Control ◽  
Necrosis Factor

Cobalamin (Cbl) deficiency causes an imbalance in some cytokines and growth factors in the central nervous system and peripheral nervous system of the rat, and in the serum and cerebrospinal fluid (CSF) of adult Cbl-deficient (Cbl-D) patients. We hypothesized that an imbalance in normal prion (PrPC) levels and/or synthesis might be involved in the pathogenesis of Cbl-D neuropathy. Using different appropriate enzyme-linked immunosorbent assays (ELISAs), we determined the levels of Cbl, tumour necrosis factor-a, epidermal growth factor, and PrPC in spinal cord (SC) and CSF of Cbl-D rats treated or not with different molecules; in serum, CSF from Cbl-D or multiple sclerosis (MS) patients; and in post-mortem SC samples taken from MS patients and control patients. We have demonstrated that: (i) Cbl deficiency induces excess PrPC regions (particularly octapeptide repeated (OR) region) in rat SC; (ii) the SC increase is mediated by a local Cbl deficiency-induced excess of tumour necrosis factor- a; and (iii) CSF and serum PrPC concentrations in Cbl-D patients are significantly higher than in controls. CSF PrPC concentrations are significantly lower in MS patients than neurological controls. The Cbl, EGF, and PrPC levels were significantly decreased in post-mortem MS SCs in comparison with controls

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