Lower levels of NAA in neurological disorders have been interpreted as reflecting neuronal cell loss, neuronal dysfunction, or altered NAA metabolism (Moffett et al., 2007). Because NAA levels can recover during recuperation following stroke, brain injury (e.g., Glodzik-Sobanska et al., 2007; Mader et al., 2008; Nakabayashi et al., 2007), and abstinence from chronic alcohol consumption (Bartsch et al., 2007; Bendszus et al., 2001; Durazzo et al., 2006; Gazdzinski et al., 2008; Parks et al., 2002), abnormally low NAA levels in these circumstances, however, likely reflect compromised neuronal “health” rather than overt neuronal death (Adalsteinsson et al., 2002).
