Alcohol consumption during pregnancy results in a range of mental and physical defects in the child which is known under an umbrella term called Fetal Alcohol Spectrum Disorder (FASD).  Prenatal Exposure to alcohol (during gestation) can drastically trigger permanent defects in physical development and memory impairment in the offspring.  The offspring who qualify for the clinical description of fetal alcohol syndrome are small for their age, reveal characteristic facial anomalies, and demonstrate noticeable deficits in central nervous system development. Rats are an accepted scientific animal model to investigate the etiopathology and novel therapeutic strategies for FASD.  Our previous studies have clearly established the neurotoxic mechanisms of FASD.  Hence, using this valid animal model, the neuroprotective effect of 7,8-dihydroxyflavone (7,8-DHF, potent agonist for Brain-Derived Neurotropic Factor (BDNF) receptor Tyrosine receptor kinase B-TrkB) was investigated.  Statistical analysis was performed using Prism-V software. 7,8-DHF significantly improved in the behavioural deficits associated with FASD by causing a significant increase in the ILK activity.