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 AB and APP immunoreactivity in the HPC. Alternatively, pharmacologically increasing expression of CRMP2 has been proposed as a possible therapeutic because it could counteract the neuronal stress associated with AD. The atypical anti-depressant, tianeptine, has a multitude of pharmacological actions, and mechanistically, it has been shown to interfere with CAMKII-GluA1 binding and pharmacologically increase CRMP expression (Hensley et al., 2011). This drug is widely prescribed for depression, yet its mechanisms of action suggest that it could be an effective candidate for the treatment of AD. Importantly, we have recently published evidence that CRMP is more abundant in the adult vs adolescent PFC proteome (Agoglia et al., 2017), we show here that CRMP is downregulated by alcohol drinking and pharmacological treatment with tianeptine can indeed reduce levels of binge drinking in adult mice (Agoglia, Sharko, et al., 2015). Future studies might investigate whether tianeptine could be effective in reversing and/or ameliorating the AD behavioral and brain pathology induced by chronic alcohol
