Our behavioral data suggest that 3xTg mice show impaired spatial learning (MWM acquisition) by 7–8months of age and that a history of moderate alcohol drinking leads to impaired short-term spatial memory (probe test). Likewise, CRMP1 KO mice show decreased LTP in CA1 and impaired acquisition of spatial learning in the Morris Water Maze as well as impaired short-term memory on a probe (Su et al., 2007). Together, these data suggest that the CRMP family of proteins may regulate some of the behavioral deficits that are observed in 3xTg mice will high likelihood of contributing to the molecular deficits. Because of its potential usefulness as an early biomarker for AD, CRMP may be a logical therapeutic target for reversing or mitigating some of the pathological and behavioral deficits associated with AD. Indeed, this hypothesis was tested by Hensley and colleagues in 3xTg mice (Hensley et al., 2013). They administered a drug that binds to CRMP2 and found that it diminished the consequences of disease progression as measured by decreased latency to find a platform in the MWM and a decrease in
