Article
Postsynaptic alteration of NR2A subunit and defective autophosphorylation of alphaCaMKII at threonine-286 contribute to abnormal plasticity and morphology of upper motor neurons in presymptomatic SOD1G93A mice, a murine model for amyotrophic lateral sclerosis.
Cerebral cortex (New York, N.Y. : 1991) - 1 Apr 2011
Spalloni A, Origlia N, Sgobio C, Trabalza A, Nutini M, Berretta N, Bernardi G, Domenici L, Ammassari-Teule M, Longone P
Abstract excerpt
Although amyotrophic lateral sclerosis (ALS) has long been considered as a lower motor neuron (MN) disease, degeneration of upper MNs arising from a combination of mechanisms including insufficient growth factor signaling and enhanced extracellular glutamate levels is now well documented. The obs...
Read the complete abstract on PubMedTopics
Share this publication in a Topic to start or enrich a Post.