{
  "abstract": "In 1956, Manchester-based neurologist Liversedge introduced the neurodegenerative disorder amyotrophic lateral sclerosis (ALS), the most common form of motor neuron disease, noting: “The origin of the disorder has been attributed to a curious medley of factors, including chill, anxiety, toxicosis, injury, and inevitably tobacco and alcohol.”1 70 years of intense epidemiological study since then has not answered this origin question definitively despite a large range of candidate factors. Observations of geographically isolated clusters of complex neurodegenerative disorders with an ALS phenotype in Guam and the Kii Peninsula focused on possible dietary neurotoxins.2 3 There has been a recurring focus on an association of athleticism in those developing ALS (see commentary Turner4), with the study of other factors, including but not limited to smoking and alcohol consumption,5 head injury,6 occupational exposures,7 military service,8 heavy metals9 and air pollution.10 Advances in the understanding of the genetic architecture of ALS11 have led to the formulation that ALS reflects interactions between external exposures and an underlying biological susceptibility.12",
  "authors": [
    {
      "affiliations": [
        "Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK"
      ],
      "name": "Christos V Chalitsios"
    },
    {
      "affiliations": [
        "Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK"
      ],
      "name": "Martin R Turner"
    }
  ],
  "title": "Considering prediagnostic environmental modifiers of progression in amyotrophic lateral sclerosis",
  "uid": "e67eb714-8f5e-5e32-a012-59d863769403"
}