@misc{Figiel_Izabela_Gene_1996,
 author={Figiel, Izabela and Filipowski, Robert K. and Hetman, Michał and Kamińska, Bożena and Kaczmarek, Leszek},
 volume={35},
 number={4},
 copyright={Creative Commons Attribution BY-SA 4.0 license},
 journal={Biotechnologia, vol.35, 4 (1996)-.},
 howpublished={online},
 year={1996},
 publisher={Committee on Biotechnology PAS},
 publisher={Institute of Bioorganic Chemistry PAS},
 language={pol},
 abstract={Excitotoxicity — cell loss occurring after an excessive neuronal stimulation with excitatoryamino acids — has been suggested to underlie major neurodegenerative disorders. Recentstudies imply that this phenomenon may have an apoptotic character, i.e., it may be an activeprocess. In our studies, reviewed herein, we confirmed and extended this view by demonstratinga gene expression component in the processes of neuronal cell loss in three different experimentalmodels: i. kainate administration, resulting in severe damage of the limbic system; ii. high-doseMK-801 treatment, evoking selective neuroned loss in the retrosplenial cortex: iii. glutamatestimulation of dentate g3Tais neurons cultured in vitro. In conclusion, we suggest that thesedata, as well as the results of a number of other studies offer a hope that there is a therapeuticwindow for the treatment of neurodegenerative diseases, both in respect to time between theinsult and cell death, and through possible common mechanisms to be targeted by futuretherapies. 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.},
 title={Gene Expression in Neuronal Apoptosis— Looking for a Therapeutic Window},
 type={Text},
 URL={http://rcin.org.pl/Content/146561/PDF/POZN271_182238_biotechnologia-1996-no4-figiel.pdf},
 keywords={biotechnology},
}