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Abstract Human genomic studies have identified protein-truncating variants in AKAP11 associated with both bipolar disorder (BD) and schizophrenia (SCZ), implicating a shared disease mechanism driven by loss-of-function

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Together, these findings indicate that HGF and possibly other growth factors hold promise for treating the neurocognitive sequela following TBI as small molecule HGF/MET activators currently in clinical trials may provide an accelerated path for testing its clinical efficacy in TBI patient populations 40

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