Our results indicate that patients with early PD have subtle signs of postural instability when their attention is diverted or reduced. In addition, deficits of stereopsis may be common in early PD patients. St Abbreviations: ACC: Accelerometers; ANOVA: Analysis of variance; AP: Antero-posterior; COP: Center of pressure; EC: Eyes closed; ECDT: eyes closed with dual task; EO: Eyes open; EODT: Eyes open with dual task; GDS: Geriatric depression scale; JERK: Jerkiness of sway; ML: Medio-lateral; MMSE: Mini mental state examination; MoCA: Montreal cognitive assessment; PD: Parkinson's disease; PDAbS: PD Patients with abnormal stereopsis; PDNrS: PD Patients with normal stereopsis; PIGD: Postural instability and gait disorder; RMS: Root mean square; UPDRS: Unified Parkinson's disease rating scale.

Stroke is the second leading cause of death worldwide. Stroke induced proliferation and differentiation of neural stem cells (NSCs) that have been proven to participate in ischemic brain repair. However, molecular mechanisms that regulate neurogenesis have not been fully investigated. MicroRNAs play an important role in the neurological repairing process and impact stroke recovery outcome. MiRNA-148b has been reported to regulate cell proliferation in tumor cells, but its role in NSCs after ischemic stroke remains unknown. Here, we found an overexpression of MiRNA-148b in subventricular zone (SVZ) of rat ischemic brain. In original cultured ischemic NSCs, transfection of MiRNA-148b mimic or inhibitor could suppress or enhance the expression of Wnt-1, β-catenin, and Cyclin D1, hence effected wnt/β-catenin signaling. MiRNA-148b inhibitor promoted NSCs proliferation and differentiation into newborn neural and astrocytes, and this action could be silenced with knockdown of Wnt-1. In middle cerebral artery occlusion (MCAo) rats, injection of MiRNA-148b inhibitor could reduce ischemic lesion volume and improve neurological function outcome. Collectively, our data suggest that MiRNA-148b suppressed wnt/β-catenin signaling attenuates proliferation and differentiation of neural stem cells, these findings shed new light on the role of MiRNA-148b in the recovery process during the stroke and contribute to the novel therapy strategy.

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