SFPQ is an abundant nuclear protein implicated in many aspects of RNA biogenesis. Importantly, nuclear depletion and cytoplasmic accumulation of SFPQ has been linked to neuropathological conditions such as Alzheimer’s disease (AD) and amyotrophic lateral sclerosis (ALS). Here we report the structural basis of cytoplasmic accumulation of SFPQ induced by zinc. The crystal structure in complex with zinc reveals the intermolecular interactions of SFPQ mediated by zinc, resulting in infinite polymerisation of SFPQ. As anticipated, the application of zinc to primary cortical neurons induced cytoplasmic accumulation and aggregation of SFPQ. Mutagenesis on the three histidine residues coordinating zinc resulted in a significant reduction in zinc-binding affinity in vitro and zinc-induced cytoplasmic aggregation of SFPQ in cultured neurons. Taken together, we propose that dysregulation of zinc in neuronal cells may represent a potential mechanism that leads to an imbalance in the nucleocytoplasmic distribution of SFPQ, an emerging hallmark of neurodegenerative diseases including AD and ALS. This study, to our best knowledge, is the first example presenting the structural basis of the Zn-induced aggregation of RNA-binding protein implicated in neurological diseases.