Antisense peptide nucleic acid targeting GluR3 delays disease onset and progression in the SOD1 G93A mouse model of familial ALS

Glutamate excitotoxicity is strongly implicated as a major contributing factor in motor neuron degeneration in amyotrophic lateral sclerosis (ALS). Excitotoxicity results from elevated intracellular calcium ion (Ca2+) levels, which in turn recruit cell death signaling pathways. Recent evidence sugge...

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Veröffentlicht in:	Journal of neuroscience research 2004-08, Vol.77 (4), p.573-582
Hauptverfasser:	Rembach, Alan, Turner, Bradley J., Bruce, Stephen, Cheah, Irwin K., Scott, Rachel L., Lopes, Elizabeth C., Zagami, Chrissandra J., Beart, Philip M., Cheung, Nam S., Langford, Steven J., Cheema, Surindar S.
Format:	Artikel
Sprache:	eng
Schlagworte:	ALS AMPA Amyotrophic Lateral Sclerosis - enzymology Amyotrophic Lateral Sclerosis - genetics Amyotrophic Lateral Sclerosis - therapy Animals antisense Antisense Elements (Genetics) - genetics Antisense Elements (Genetics) - metabolism Antisense Elements (Genetics) - pharmacology Calcium - metabolism Calcium - toxicity Calcium Signaling - drug effects Calcium Signaling - physiology Cell Death - drug effects Cell Death - genetics Cells, Cultured Disease Models, Animal Disease Progression Down-Regulation - drug effects Down-Regulation - genetics Excitatory Amino Acid Agonists - pharmacology Excitatory Amino Acid Antagonists - pharmacology excitotoxicity GluR3 Mice Mice, Transgenic Nerve Degeneration - enzymology Nerve Degeneration - genetics Nerve Degeneration - therapy NSC-34 cell Peptide Nucleic Acids - pharmacology PNA Receptors, AMPA - antagonists & inhibitors Receptors, AMPA - genetics Receptors, AMPA - metabolism SOD1 Superoxide Dismutase - genetics Superoxide Dismutase - metabolism Survival Rate
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