Recently, Rothstein et al. reported that beta-lactam antibiotics, including 
penicillin and ceftriaxone, are potential therapeutic drugs to treat some 
neurological disorders, e.g., amyotrophic lateral sclerosis (ALS), by modulating 
the expression of glutamate transporter GLT1 via gene activation. However, 
considering the facts that: (i) many neurological diseases (including ALS) are 
associated with transition metal ions and redox stress, and ALS can be 
efficiently prevented by metal chelators, e.g., diethyl-dithiocarbamate (DDC); 
(ii) beta-lactam antibiotics have long been known as metal chelators, we argue 
that the beneficial effect of beta-lactam antibiotics on ALS likely involves 
Cu(II)-attenuating ability. This is partially supported by our theoretical 
calculations.