Bid signal pathway components are identified in the temporal cortex with Parkinson disease

Hong Jiang, Ping He, Charles H. Adler, Holly Shill, Thomas G. Beach, Rena Li, Yong Shen

Research output: Contribution to journalArticlepeer-review

11 Scopus citations

Abstract

Objective: Parkinson disease (PD), a devastating neurodegenerative disorder, affects motor abilities and cognition as well. It is not clear whether the proapoptotic protein, Bid, is involved in tumor necrosis factor death receptor I (TNFRI)-mediated destructive signal transduction pathways such as cell dysfunction or neurodegeneration in the temporal cortex of patients with PD. Methods: Molecular and biochemical approaches were used to dissect mitochondrial related components of the destructive signaling pathway in the temporal cortex from rapidly autopsied brains (postmortem interval mean 2.6 hours). Brains from patients with PD (n = 15) had an average age of 81.4 years, compared to the average age of 84.36 years in age-matched control patient brains (n = 15). Results: TNFRI and its adaptor protein, TRADD, were not only present in the cytoplasm of the temporal cortex, but were significantly elevated (42.3% and 136.1%, respectively) in PD brains compared to age-matched control brains. Bid in the PD temporal cortex could be further cleaved into tBid in the cytosol, which is translocated into the mitochondria, where cytochrome c is then released and caspase-3 is subsequently activated. Conclusion: Patients with PD have an activated Bid-mediated destructive signal pathway via TNFRI in the temporal cortex. Such deficits are pervasive, suggesting that they might contribute to cortex degeneration as PD manifests.

Original languageEnglish (US)
Pages (from-to)1767-1773
Number of pages7
JournalNeurology
Volume79
Issue number17
DOIs
StatePublished - Oct 23 2012

ASJC Scopus subject areas

  • Clinical Neurology

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