Our previously published [3, 10, 11] cohort is composed of individuals stratified by clinical and pathological features across a range of disease subtypes (sporadic ALS, ALS-SOD1 and ALS-C9orf72), in brain regions associated with cognitive function (executive, language and fluency), and cognitive symptom presentations (with or without cognitive deficits measured during life using the Edinburgh Cognitive ALS Screening tool). This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.