Schizophrenia is a prevalent and serious mental illness with a lifetime prevalence of about 1% (Saha et al., 2005). This condition is characterized by a range of psychotic symptoms that can be broadly categorized into cognitive, positive, and negative symptom clusters. Cognitive symptoms often manifest as impairments in working memory, executive function, and processing speed. Positive symptoms are typified by delusions and hallucinations, while negative symptoms involve a lack of motivation and social withdrawal. In many cases, social and occupational abilities are reduced, and SCZ is also associated with reduced life expectancy. The average life expectancy of people with schizophrenia is about 15 years less than that of the general population, and the risk of suicide death over time ranges from 5% to 10% (Hjorthøj et al., 2017). Meanwhile, the impact of SCZ extends beyond the individual patient to families and society.

So far, the exploration of the etiological mechanism of SCZ remains a challenge. Notably, the onset of schizophrenia often occurs during early adulthood, yet its origins can be traced back to the early stages of neurodevelopment. (Murray and Lewis, 1988). The role of early life environment and genetic risk factors in altering the trajectory of neurodevelopment can disrupt brain development, particularly in certain neuronal subtypes and brain regions, thereby increasing an individual's risk of SCZ and leading to the development of prodromal symptoms. This evidence includes a rise in obstetric problems such as preterm birth and pre-eclampsia as well as intrauterine adversities, such as maternal illnesses throughout pregnancy (Bramon et al., 2005; Hulshoff Pol et al., 2000).

Numerous molecules collaborate geographically and temporally throughout neurodevelopment to enable the complete construction of the organism (Díaz et al., 2014). miRNAs are small non-coding RNA molecules that negatively regulate gene expression and are widely involved in cell proliferation, differentiation, apoptosis, and cell cycle regulation. Approximately 70% of miRNAs are expressed in the central nervous system (CNS)(Krichevsky et al., 2003)。Let-7 and miR-18 families have been linked to mESC ectodermal and mesodermal differentiation by targeting Acvr1b and Smad2, according to studies by Colas AR et al. (Colas et al., 2012) The signaling pattern that decides whether a cell becomes an ectoderm and the fate of the mesoderm is triggered by the downregulation of these targets, which also results in diminished nodal reactivity. Du ZW et alconfirmed that during the differentiation of neuroectodermal precursors, human embryonic stem cells (ESC) down-regulated miR-200 and miR-96 families, and overexpressed target ZEB transcription factors and Pax6, which inhibited neural induction (Du et al., 2013). In addition, miR-124 (Gu et al., 2023; Sun and Shi, 2015)，miR-9 (Zhao et al., 2013)，miR-137 (Sun et al., 2011)，miR-219 (Dugas et al., 2010)，miR-132 (Hancock et al., 2014)，miR-17 family (Bian et al., 2013; Chen et al., 2011)，miR-195 (Liu et al., 2013) which are well known to us, have been confirmed to be involved in the regulation of neural stem cells proliferation, neurogenesis, neuronal migration, neurite growth and synaptic formation by regulating their target genes.

Methodologically, the role of miRNAs in central nervous system development and neurogenesis is being explored through a variety of experimental designs, such as the use of Dicer conditioned deletion mice or Dicer knock-out of ESC, inhibition of its level of expression during central nervous system development, and reduction of its function by interfering with its binding to target mRNA.

Even so, the function of a sizable number of miRNAs has not yet been established, and their involvement in neurodegenerative illnesses like schizophrenia remains poorly known. In our previous study, we found that the expression level of miR-30e-3p in the peripheral blood of SCZ patients who were first untreated was only 0.32 times that of healthy controls, and verified that its target gene ABI1 was significantly up-regulated in SCZ patients.

miR-30e-3p is associated with susceptibility to neuropsychiatric diseases, and the miR-30e-3p target gene group is significantly enriched in the PI3K-Akt pathway. Decreased activity of the PI3K-Akt signaling pathway may partially explain cognitive impairment, abnormal synaptic morphology, neuronal atrophy, and neurotransmitter signaling dysfunction in schizophrenia patients (Zheng et al., 2012). ABI1, also known as E3B1. Scita et al. confirmed that ABI1 can participate in Ras and P13K signaling pathways, activate Rac, and promote actin polymerization and cytoskeletal reconstruction (Scita et al., 2001). The initiation, growth and branching of neurites are influenced by actin and microtubule cytoskeleton (Dent et al., 2007; Mattila and Lappalainen, 2008). Therefore, we hypothesize that miR-30e-3p interacts with patients' neurodevelopmental processes through ABI1 and is involved in the etiological mechanism of SCZ. In this study, we first summarized and predicted the temporal and spatial expression patterns of ABI1 in brain tissues and cells by using public databases, and then explored the contribution of miR-30e-3p and ABI1 to cellular neurodevelopment by using differentiated SH-SY5Y cells through a series of experiments.