Neuromics, the analysis of genomic DNA for risk association with a neurological disease, has achieved considerable success recently. An increased risk for amyotrophic lateral sclerosis (ALS), Alzheimer disease (AD), restless leg syndrome (RLS), and multiple sclerosis has been associated with polymorphisms in specific genes. These observations are truly significant advances in the appreciation of the causation of inherited, complex polygenetic, multifactorial neurological diseases. They have been made possible by the publication of the human genome and haplotype studies (HapMap analyses). Neurome-wide association studies will increase in the future and we plan on devoting an increased interest in them, as they provide a new detailed level of analyses to achieve a clearer understanding of multigene interactions responsible for neurological disease. For the time being, most of these neurome-wide analyses will not have direct clinical relevance and will not directly affect patient care. Eventually, and perhaps quite soon, they will at least provide a risk assessment to monitor specific patients in large pedigrees for their risk of disease presentation. Pharmacogenomics, or more specifically, pharmaconeuromics, will be an early positive result by initiating the design of specific drug therapies for a patient's neurological disease based on his or her neuromic risk.1
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