Barkats M, Bertholet J Y, Venault P, Ceballos-Picot I, Nicole A, Phillips J, Moutier R, Roubertoux P, Sinet P M, Cohen-Salmon C
URA 1294 CNRS, UFR Biomédicale des Saints Pères, Paris, France.
Neurosci Lett. 1993 Sep 17;160(1):24-8. doi: 10.1016/0304-3940(93)90908-4.
The copper-zinc superoxide dismutase (SOD-1) gene, located on chromosome 21 and triplicated in Down's syndrome (DS), is suspected to be involved in the neuropathology observed in Alzheimer's disease (AD), DS and physiological aging. In order to explore the effect of an overproduction of SOD-1 in the mouse hippocampus, we investigated the Timm-stained mossy fiber (MF) innervation in the hippocampus of transgenic mice for the human SOD-1 gene (hSOD-1 mice). The results showed a decrease of the MF projection area in the hSOD-1 mice overexpressing the SOD-1 protein. These findings suggest that free radicals could play a role in this particular synaptic loss.
