TTR and Abnormal autonomic nervous system physiology: Transthyretin mutations result in the deposition of amyloid fibrils in the peripheral and autonomic nerves, gastrointestinal tract and myocardium, typically presenting with an axonal predominant, length-dependent sensorimotor polyneuropathy (thus, the disorder is also termed familial amyloid polyneuropathy, FAP [2]) that frequently coexists with autonomic dysfunction, cardiac involvement and weight loss [9].