The Therapeutic Potential of the Novel Player Kcnn2 in Fetal Alcohol Syndrome Disorder Pathogenesis Sofia Tiu
One of the leading contributors to disability within fetal development is alcohol, affecting 3% of all newborn children.1 Fetal alcohol spectrum disorders (FASD) is an umbrella term that is used for a set of disorders that arise by prenatal alcohol exposure (PAE) administered by a pregnant mother.2 Main FASD treatments currently rely on cognitive-behavioural treatments due to the lack of medications.3 Although the effects of these therapies have been well studied, there is ongoing research for more biological advances into discovering FASD pathogenesis. Currently, FASD pathogenesis has observed that PAE affects certain downstream neurodevelopmental pathways which lead to amplified consequences, such as excessive cell death and proliferation and modified cell signaling affecting gene expression.4 A recent study by Mohammad et al. indicates that increased expression of Kcnn2 is associated with motor learning disability in CD-1 FASD mice models.5 Furthermore, Kcnn2knockdown PAE mice express higher levels of motor learning in earlier adulthood compared to PAEmice with increased Kcnn2 expression.5 Investigation into this Kcnn2-motor pathway has indicated that inhibiting Kcnn2 channels increases motor cortex activation and decreases motor symptoms in a FASD mouse model, indicating that Kcnn2 inhibition may be a novel route for treating FASD motor progression in humans.5 Key words: Fetal Alcohol Syndrome Disorder (FASD), prenatal alcohol exposure (PAE), Kcnn2, motor learning, CD-1 mice model
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