2010). If and how these traits may potentially contribute to SJL × C57/B6 strain-specific onset/progression and drug response characteristics in hSOD1 transgenics is unclear. In conclusion, the present data indicate that galectin(s)-3 and -9 are increased in ALS and an SOD1G93A mouse model of ALS. Galectin-3 is primarily expressed by microglia in the SOD1G93A mouse model of ALS, and in humans with ALS. Deletion of galectin-3 in the SOD1G93A Inhibitors,research,lifescience,medical mouse resulted in rapid disease progression, and increases in microglia, TNF-α,

and oxidative injury, compared with galectin-3 expressing SOD1G93A diseased controls. Thus, endogenous production of galectin-3 by microglia may, at least in part, serve to limit mTOR inhibitor neuroinflammation and disease progression during chronic motor neurodegenerative disease. Acknowledgments This work was partially supported by National Institutes of Health/National

Institute of Neurological Disorders and Stroke NS041679, National Institutes of Health/National Inhibitors,research,lifescience,medical Center for Medical Rehabilitation Research/National Institute of Neurological Disorders and Stroke 2R24HD050846-06 (NCMRR-DC Core Molecular and Functional Outcome Measures in Rehabilitation Medicine), and National Institutes of Health/National Institute of Neurological Disorders and Stroke 5R01NS029525 (Intellectual and Developmental Disabilities Research Center 1P30HD40677-06). Contents are solely the responsibility of Inhibitors,research,lifescience,medical the authors and do not necessarily represent the official views of the National Institutes of Health. Conflict of Interest The authors declare no conflict(s) of interest.
Humans Inhibitors,research,lifescience,medical vary considerably in their ability to delay gratification and maladaptive levels of impulsive decision making are a common feature in various psychiatric disorders, including substance use disorder, attention deficit hyperactivity disorder (ADHD),

conduct disorder, bipolar disorder, Inhibitors,research,lifescience,medical and pathological gambling (Moeller et al. 2001). Impulsive decision making is reflected by an increased preference for (smaller) immediate rewards over (larger) delayed rewards and often assessed by delay discounting paradigms. Impulsive decision making is a relatively stable psychological trait that is at least partly attributable to genetic differences, although Phosphoprotein phosphatase state-dependent shifts from baseline (trait) levels can occur (for a review see Peters and Buchel 2011). Given the trait-like characteristics of impulsive decision making, it can be argued that individual differences in delay discounting can be predicted by intrinsic properties of brain functioning, such as brain metabolites and spontaneous fluctuations in blood oxygen level-dependent (BOLD) activity. In recent years, considerable progress has been made in unraveling the underlying neurobiology of impulsivity. On a molecular level, various neurotransmitter systems have been implicated in impulsive decision making (Winstanley et al. 2006; Pattij and Vanderschuren 2008).