In Schistocerca americana, the DCMD has been shown to synapse onto motoneurons responsible for evoking escape behaviors (Fotowat et al., 2011), although its effect on other muscle groups is not known.
MMP-7 has also been shown to modulate synapse morphology.
The synapse and dendritic spine loss are strongly correlated with cognitive impairment in AD, and A β has been shown to target synapses [ 40, 50].
Insulin in fact has recently been shown to protect synapses against Aβ oligomers [25].
Moreover, NRG1 has been shown to promote excitatory synapse development in GABAergic interneurons [ 11].
AP-1 has also been shown to positively regulate synapse strength and number, acting upstream of CREB [ 67].
Golgi cells have previously been shown to receive inhibitory synapses from both Lugaro and other Golgi cells in the cerebellar cortex.
Since misfolded tau has been shown to transmit across synapses in AD animal models, we hypothesized that synapses in AD patients may contain misfolded tau.
Indeed, amyloid oligomers have been shown to bind preferentially to synapses [ 223].
Dynein and its associated dynactin complex have been shown to be important for synapse formation and stabilization in both Drosophila and C. elegans [17], [11], [19], [20].
