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A rare polymalformative syndrome characterized by agenesis of corpus callosum (CC), distal anomalies of limbs, minor craniofacial anomalies and intellectual disability.
Upregulation of SUFU (Suppressor of Fused) expression to restore GLI3 processing and normalize SHH signaling gradient formation during early neural tube development, promoting commissural axon guidance and corpus callosum formation
Pharmacological upregulation of Netrin-1 secretion from floor plate cells and enhancement of DCC (Deleted in Colorectal Cancer) receptor sensitivity to promote commissural axon crossing and potentially stimulate compensatory interhemispheric connections
Dual targeting of GSK3β (by lithium) and HDACs (by valproic acid) to enhance WNT/β-catenin signaling while promoting chromatin remodeling, potentially reactivating developmental programs for neural connectivity and digit morphogenesis
Viral vector-mediated IGF-1 overexpression in oligodendrocyte precursor cells to promote their proliferation and differentiation via PI3K/AKT/mTOR pathway activation, supporting white matter tract development and myelination in residual interhemispheric connections
Bacoside A and bacosides from Bacopa monnieri activate CREB phosphorylation leading to increased BDNF expression, promoting synaptic plasticity and potentially compensating for developmental corpus callosum defects through enhanced interhemispheric connectivity
Gastrodin from Gastrodia elata promotes GABA receptor expression while shifting microglia from M1 to M2 phenotype via STAT6 activation, reducing neuroinflammation and supporting late-stage neuroplasticity in acrocallosal syndrome patients