Abstract

We read with interest the recent article “TDP-43 proteinopathy and motor neuron disease in chronic traumatic encephalopathy” by McKee et al (1). As neuromuscular specialists who care for large numbers of patients with amyotrophic lateral sclerosis (ALS), we have concerns about the conclusions drawn from 3 cases diagnosed as having ALS in life, while having histologic changes of both ALS and chronic traumatic encephalopathy (CTE) at autopsy. In their 12-paragraph discussion section and subsequent New York Times interview (2), the authors propose a cascade of events starting with head trauma, leading to TDP-43 proteinopathy, and ultimately to various clinical phenotypes including motor neuron disease. In support of this, they state, “… of all the putative environmental risk factors, trauma to the CNS emerges as one of the strongest and most consistent contenders for initiating the molecular cascades that result in ALS.” In actuality, the data linking trauma to ALS are significantly …

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