Loss of sorting nexin 27 contributes to excitatory synaptic dysfunction by modulating glutamate receptor recycling in Down's syndrome"Here we demonstrate a new role for SNX27 in the dysregulation of synaptic function in Down's syndrome. We show that chromosome 21–encoded miR-155 targets and downregulates C/EBPβ, which is a transcription factor for SNX27. Thus, the lower amounts of C/EBPβ in Down's syndrome lead to reduced SNX27 expression. We show that SNX27 promotes recycling of AMPARs and NMDARs from early endosomes to the plasma membrane through direct PDZ binding and thus prevents their degradation. Deletion of Snx27 in mice results in synaptic dysfunction and cognitive deficits. Further, overexpressing Snx27 in the hippocampus of Ts65Dn mice reverses the impairments in receptor amounts and synaptic functions, as well as in hippocampus-dependent memory. Therefore, SNX27 is crucial for maintaining glutamate receptors through post-translational mechanisms and is required for normal synaptic activity and memory formation."
Of course, I went looking for a way to increase the expression of SNX 27 and in a matter of days I found it. I love the internet!
In Slesinger Lab at the Salk Institute, they are studying SNX27 and other parts of the signalling pathways. They found that Stimulants up regulated SNX27. I think ADHD meds qualify as a stimulant.