Fig. 1.

Involvement of ProSAP/Shank scaffold Zn²⁺-induced modulation of synaptic (dys)function in ASD. Zn²⁺ supplementation was shown to increase SHANK2 recruitment to synapses, modulate postsynaptic NMDAR currents (Fourie et al., 2018), increase Shank gene expression, and improve synaptic density (Hagmeyer, Mangus, Boeckers, & Grabrucker, 2015), altogether resulting in improved social interaction and reduced autism-like repetitive and anxiety behaviors (Fourie et al., 2018; Lee et al., 2015). Furthermore, Zn deficiency is associated with altered synapse plasticity, formation, and maturation (Grabrucker, 2014; Grabrucker et al., 2014).