Previous work from our laboratories and other groups has shown that the PD-associated kinase LRRK2 regulates important synaptic processes (Beccano-Kelly et al., 2014; Beccano-Kelly et al., 2015; Chen et al., 2025c). At the postsynapse, LRRK2 modulates the function of excitatory synapses in the striatum (Chen et al., 2020; Matikainen-Ankney et al., 2016; Tong et al., 2009; Volta et al., 2017; Beccano-Kelly et al., 2015; Xenias et al., 2022). LRRK2 was previously reported to interact with Rac1 (Chan et al., 2011; Feng et al., 2018) and with other actin-related proteins (Meixner et al., 2011). It has been shown that drebrin knockout results in delayed synaptogenesis and inhibition of postsynaptic PSD95 accumulation, indicating its key role in spine maturation (Koganezawa et al., 2017; Takahashi et al., 2003; Aoki et al., 2009). Indeed, striatal Lrrk2 expression in the rodent brain increases up to postnatal week 4 (Parisiadou et al., 2014; Westerlund et al., 2008; Biskup et al., 2007; Cogo et al., 2022), while the Lrrk1 transcript in this region remains relatively stable during development (Westerlund et al., 2008).