BACKGROUND: Multiple system atrophy (MSA) and Parkinson's disease (PD) patients develop respiratory and cardiovascular disturbances including obstructive sleep apnea, orthostatic hypotension, and nocturnal stridor. We hypothesized that, associated with these respiratory and cardiovascular disturbances, hypoxic events may occur in MSA and PD brains that may play a role in disease progression. The objective of this study was to evaluate the presence of hypoxia in nonneurological controls and PD and MSA patients. METHODS: Molecular levels of hypoxia markers were measured in postmortem brain tissue from controls and PD and MSA cases. RESULTS: MSA brain showed signs of chronic hypoxia characterized by the significant accumulation of the hypoxic marker HIF2α as compared to PD patients and controls. We detected no differences between MSA subtypes. Signs of hypoxia were also observed in PD patients with a clinical presentation similar to the MSA cases. CONCLUSIONS: The results obtained from this study suggest a new alternative pathway associated with α-synucleinopathies that may contribute to the pathogenesis of these disorders.
BACKGROUND: Multiple system atrophy (MSA) and Parkinson's disease (PD) patients develop respiratory and cardiovascular disturbances including obstructive sleep apnea, orthostatic hypotension, and nocturnal stridor. We hypothesized that, associated with these respiratory and cardiovascular disturbances, hypoxic events may occur in MSA and PD brains that may play a role in disease progression. The objective of this study was to evaluate the presence of hypoxia in nonneurological controls and PD and MSA patients. METHODS: Molecular levels of hypoxia markers were measured in postmortem brain tissue from controls and PD and MSA cases. RESULTS: MSA brain showed signs of chronic hypoxia characterized by the significant accumulation of the hypoxic marker HIF2α as compared to PDpatients and controls. We detected no differences between MSA subtypes. Signs of hypoxia were also observed in PDpatients with a clinical presentation similar to the MSA cases. CONCLUSIONS: The results obtained from this study suggest a new alternative pathway associated with α-synucleinopathies that may contribute to the pathogenesis of these disorders.
Authors: Robert M Douglas; Julie Ryu; Amjad Kanaan; Maria Del Carmen Rivero; Laura L Dugan; Gabriel G Haddad; Sameh S Ali Journal: Am J Physiol Cell Physiol Date: 2010-03-31 Impact factor: 4.249
Authors: Jayasri Nanduri; Ning Wang; Guoxiang Yuan; Shakil A Khan; Dangjai Souvannakitti; Ying-Jie Peng; Ganesh K Kumar; Joseph A Garcia; Nanduri R Prabhakar Journal: Proc Natl Acad Sci U S A Date: 2009-01-14 Impact factor: 11.205
Authors: Axel Lipp; Paola Sandroni; J Eric Ahlskog; Robert D Fealey; Kurt Kimpinski; Valeria Iodice; Tonette L Gehrking; Stephen D Weigand; David M Sletten; Jade A Gehrking; Kim K Nickander; Wolfgang Singer; Demetrius M Maraganore; Sid Gilman; Gregor K Wenning; Clifford W Shults; Phillip A Low Journal: Arch Neurol Date: 2009-06
Authors: Tetsutaro Ozawa; Dominic Paviour; Niall P Quinn; Keith A Josephs; Hardev Sangha; Linda Kilford; Daniel G Healy; Nick W Wood; Andrew J Lees; Janice L Holton; Tamas Revesz Journal: Brain Date: 2004-10-27 Impact factor: 13.501