Dyslipidemia in ALS

Recent research suggests that amyotrophic lateral sclerosis (ALS) involves metabolic alterations, most notably increased rates of energy expenditure, in addition to degeneration of motor neurons.1 For example, animal models of ALS demonstrate increased rates of energy expenditure. In these models, calorie restriction exacerbates motor symptoms, and increased lipid content in diets is associated with neuroprotection and extended survival. These studies suggest that lipid status may change with ALS and that alterations in metabolism may be a cardinal feature of the disease. In this issue of Neurology ®, Dupuis et al.2 investigate these issues by examining plasma cholesterol in a large series of patients with ALS relative to healthy controls; they also examined hepatic steatosis in patients with ALS and patients with Parkinson disease (PD). In both comparisons, people with ALS were significantly more likely to show evidence of hyperlipidemia. Mean low-density lipoprotein …