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Pro-inflammatory cytokine TNF-alpha as a neuroprotective agent in the brain

100%
Figiel I.
Acta Neurobiologiae Experimentalis
|
2008
|
vol. 68
|
issue 4
526-534
EN
Despite the numerous reports on the role of tumor necrosis factor-alpha (TNF-alpha) in the brain neuropathology, very little is known about the mechanisms by which TNF-alpha may mediate neuroprotection. Different hypotheses pertain to the molecular and cellular effectors triggered by the activation of TNF receptors (TNFRI and TNFR2). They are focused on diminishing the production of nitric oxide and free radicals, alteration of excitatory amino acids neurotransmission, maintenance of neuronal calcium homeostasis and induction of neurotrophic factors synthesis. In this review all these data are summarized. Moreover, possible explanations for the inconsistent data concerning the TNF-alpha effect on neuron are discussed.
2

Gene expression in neuronal apoptosis-looking far a therapeutic window

51%
Figiel I., Filipkowski R. K., Hetman M. K. B., Kaczmarek L.
Biotechnologia
|
1996
|
issue 4
132-140
EN
Wxititixicity - cell loss occurring after an excessive stimulation with excitatory amino acid - has been suggested to underlie major neurodegenerative disorders.Recent studies imply that this phenomenon may have an apoptotic character, i.e.., it may be an active process.In our studies, revived herein, we confirmed and extended this view by demonstratijng a gene expression component in the processes of neuronal cell loss in three different experimental models: i. kinate administration, II, high-dose MK-801 treatment, iii.glutamate stimulation of dentate gyrus neurons cultured in vitro.In conclusion we suggest that these data, as well as tha results of a number of other studies offer a hope that there ia a therapeutic window for the treatment of a neurodegenerative diseases, both in respect to time between the insult and cell death, and through possible common mechanisms to be targeted by future therapies.One can even speculate that such therapies might aim at transcription factors, e.g. AP-1 of a specific composition and/or executor hydrolytic enzymes, e.g., cathepsin D.
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