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Down syndrome (DS) is the most common genetic cause of mental retardation. In DS there is a glial deficit which induces anomalies in neurotrophins, including Activity Dependent Neuroprotective Protein and Activity Dependent Neurotrophic Factor. Previously we have shown that their active fragments NAP+SAL prevented delay in behavioral milestones achievement in the Ts65Dn (Ts) mouse, a DS model. The objective of this study was to test if NAP+SAL prevent the adult DS learning deficit.
9-12 month old Ts male mice were treated for 10 consecutive days with either D-NAP+D-SAL or placebo. From treatment day 4 mice were tested for learning on the Morris watermaze for 5 days where latency to find a hidden platform by using visual cues is a measure of learning. Probe tests for long term memory were performed on treatment day 9 and 10 days later (after treatment stopped). Statistics included Bonferroni-Dunn with P<0.05 significant.
15 Control, 4 Ts and 9 Ts+NAP+SAL were tested. Ts animals did not learn (P<0.001) over the 5-day period vs the control. Ts animals treated with NAP+SAL learned significantly better than the Ts mice (P<0.001, Figure). On treatment day 9 Ts+NAP+SAL retained learning, with results similar to the controls (P>0.05). However, 10 days after therapy, Ts+NAP+SAL did not maintain learning in the probe test.
Postnatal treatment with peptides NAP+SAL prevented learning deficit in a model for DS. Possible mechanisms of action include overcoming the glial deficit.