In a recent study published in Signal Transduction and Targeted Therapy, Liu et al. [1] studied a particular circuit from lobules IV/V in the cerebellar vermis to neurons within the fastigial nucleus (FN), which regulates sensorimotor coordination. They also identified biorientation defective 1 (BOD1) as part of the molecular mechanism of the circuit, in which a deficit in Purkinje cells (PCs) in lobules IV/V triggers hyperactivation in FN CaMKIIα+-neurons, resulting in behavioral signs of ataxia (Fig. 1).
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