Causes of death in multiple system atrophy

We present our results from a study on the causes of death in a series of pathologically confirmed, definite Multiple system atrophy cases

S. Papapetropoulos; A. Tuchman; D. Laufer; A. G Papatsoris; N. Papapetropoulos; D. C Mash

2007

Scholarcy highlights

  • Our data support the hypothesis that the change in iron metabolism may confer susceptibility to neurodegenerative diseases such as ALS
  • The exon 2 polymerase chain reaction product is used for S65C and H63D polymorphisms, and the exon 4 PCR product for the C282Y mutation
  • In a human neuronal cell line transfected with genes carrying the HFE mutations, the H63D polymorphism induced a decreased expression of SOD1, a-tubulin and b-actin; these events can cause a disruption of axonal transport, a factor implicated in ALS pathogenesis
  • Further studies on the analysis of iron metabolism in patients with ALS are needed to elucidate the role of the H63D polymorphism as a genetic risk factor for sporadic ALS
  • We present our results from a study on the causes of death in a series of pathologically confirmed, definite Multiple system atrophy cases
  • All patients registered with the University of Miami/NPF Brain Endowment Bank donation programme with a diagnosis of neuropathologically confirmed, definite multiple system atrophy were included in this study
  • All patients with Multiple system atrophy died from disease-related events, with sudden death and infections being the most common

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