Biomedical subjects

J-M Warter

Publications and source records attributed to J-M Warter.

4 recordsLinked to original sources

PubMed2005

[Interferon beta1-a IM once weekly does not modify general psychological function in the first months after therapy in patients with relapsing-remitting multiple sclerosis].

INTRODUCTION: Psychological troubles are common in multiple sclerosis but their underlying etiology is still controversial. METHODS: The objective of this open, non comparative, multicenter study was to assess changes in global psychological functioning in new multiple sclerosis patients during the first 3 months of treatment with intramuscular interferon beta-1a once weekly (Avonex). This functioning was rated every 4 weeks with the GAF (Global Assessment Functioning) scale. Depression measured on MADRS (Montgomery & Asberg Depression Rating Scale), clinical global impression (CGI) on patients'psychological status and clinical as well as biological tolerance were also assessed every 4 weeks. RESULTS: Five hundred and ninety-nine patients (71.4 percent women), aged 39.4 years were included. No clinically significant difference in mean GAF score between baseline and the end of the first 3 months of interferon beta-1a IM treatment (main evaluation outcome) was found. Similar results were obtained on MADRS scale. CONCLUSION: No clinically significant alteration of global psychological functioning, including symptoms of depression, was observed during the first 3 months of treatment with interferon beta-1a IM.

Adjuvants, Immunologic↗

PubMed2003

[Lyme borreliosis].

Lyme disease is a multisystemic disease caused by a spirochete, Borrelia Burgdorferi that is transmitted by ticks. A clinical diagnosis is easy when a tick bite is followed 3 weeks later by erythema migrans, than by involvement of nervous system, joints or heart. In case of neuroborreliosis, serological tests, performed in blood and cerebro-spinal fluid, support the diagnosis and patients recover rapidly with antibacterial treatments. However an accurate diagnosis remains sometimes problematic, especially distinction between a coincidental positive serologic test and a nervous system Lyme borreliosis which require antibiotics. Furthermore, the role of autoimmunity in the pathophysiology of late Lyme disease, antibiotic choice in early disease, duration of treatment, and utility of vaccination are discussed.

Animals↗

PubMedDate not supplied

Quantification of neurotrophin mRNA expression in PMN mouse: modulation by xaliproden.

Compounds possessing neurotrophic properties may represent a possible treatment for neurodegenerative disorders such as amyotrophic lateral sclerosis. Xaliproden (SR57746A), an orally-active non-peptide compound, which has been found to exhibit neurotrophic effects in vitro and in vivo, increased the lifespan and delayed the progression of the motor neuron degeneration in PMN mice. We have used a quantitative reverse transcription/polymerase chain reaction amplification technique to study the regulation of neurotrophin mRNA and trk mRNA expression in PMN mice. NGF and NT-3 mRNA are downregulated in PMN mice. These deficiencies can be overcome by a treatment with xaliproden. Such an effect could contribute to neurotrophic effects of xaliproden in vivo and in vitro.

Animals↗

PubMedDate not supplied

Xaliproden (SR57746A) induces 5-HT1A receptor-mediated MAP kinase activation in PC12 cells.

Neurotrophic growth factors are involved in cell survival. However, natural growth factors have a very limited therapeutic use because of their short half-life. In the present study, we investigated the mechanism of action of a non-peptidic neurotrophic drug, Xaliproden, a potential molecule for the treatment of motoneuron diseases, since the transduction pathways of this synthetic 5-HT1A agonist are very poorly understood. Xaliproden does not activate the Trk receptor but causes a rapid increase in the activities of the ERK1 and ERK2 isoforms of MAP kinase, which then rapidly decrease to the basal level. We demonstrate that isoforms of the SHC adapter protein are phosphorylated independently of each other and are probably not the source of the Xaliproden-induced MAP kinases activation. The inhibitor of Ras farnesylation, FPT-1, and the protein kinase C inhibitors, GF 109203X and chelerythrine, inhibited the Xaliproden-induced MAP kinase activation, suggesting p21Ras and PKC involvement. Moreover, the observations that the 5-HT1A antagonist, pindobind, and pertussis toxin abolished the Xaliproden-induced ERK stimulation suggested that Xaliproden activates the MAP kinase pathways by stimulating the G protein-coupled receptor, 5-HT1A. These results demonstrate clearly that the non-peptidic compound, Xaliproden, exerts its neurotrophic effects through a mechanism of action differing from that of neurotrophins. These findings suggest that this compound does not involve MAPK activation by TrkA receptor stimulation but acts by MAP kinase pathway by a pertussis toxin-sensitive mechanism involving 5-HT1A receptors, p21 Ras and MEK-1 and by PKC and Akt pathways.

Adaptor Proteins, Signal Transducing↗