Inhibition of calpains improves memory and synaptic transmission in a mouse model of Alzheimer disease

• Published in: The Journal of clinical investigation Vol. 118; no. 8; pp. 2796 - 2807
• Main Authors: Trinchese, Fabrizio, Fa’, Mauro, Liu, Shumin, Zhang, Hong, Hidalgo, Ariel, Schmidt, Stephen D., Yamaguchi, Hisako, Yoshii, Narihiko, Mathews, Paul M., Nixon, Ralph A., Arancio, Ottavio
• Format: Journal Article
• Language: English
• Published: United States American Society for Clinical Investigation 01.08.2008
• Subjects: Alzheimer Disease - drug therapy; Alzheimer Disease - metabolism; Alzheimer Disease - physiopathology; Alzheimer's disease; Animals; Biomedical research; Calpain; Calpain - antagonists & inhibitors; Cell culture; Cells, Cultured; Control; Cyclin-dependent kinases; Disease Models, Animal; Enzymes; Glycoproteins - pharmacology; Hippocampus - cytology; Hippocampus - metabolism; Homozygote; Immunohistochemistry; Kinases; Leucine - analogs & derivatives; Leucine - pharmacology; Localization; Memory; Memory - drug effects; Mice; Mice, Transgenic; Models, Neurological; Neural transmission; Peptides; Phosphorylation; Physiological aspects; Proteins; Synaptic Transmission - drug effects; United States

Calpains are calcium-dependent enzymes that determine the fate of proteins through regulated proteolytic activity. Calpains have been linked to the modulation of memory and are key to the pathogenesis of Alzheimer disease (AD). When abnormally activated, calpains can also initiate degradation of pro...