About this item:

598 Views | 0 Downloads

Author Notes:

Correspondence: Ranjita Betarbet, Address: Center for Neurodegenerative diseases, Emory University, Whitehead Biomedical Research Building, Room 505M, 615 Michael Street, Atlanta, GA 30322; Phone: 404-727-9216; Fax: 404-727-3728; Email: rbetarb@emory.edu

Acknowledgments: The authors would like to thank deCODE Genetics, Reykjavík, Iceland, for the kind gift of the FAF1 antibody and for discussions.


Research Funding:

This work was supported by Close to A Cure funding agency (RB) and NIEHS grants ES012068 (AIL) & ES015777 (RB).


  • PARK 10
  • cell death
  • oxidative stress
  • α-synuclein
  • mitochondrial inhibition

Fas Associated Factor 1 and Parkinson’s disease


Journal Title:

Neurobiology of Disease


Volume 31, Number 3


, Pages 309-315

Type of Work:

Article | Post-print: After Peer Review


Fas-associated factor 1 or FAF1 is a Fas binding protein implicated in apoptosis. FAF1 is the product of a gene at PARK 10 locus on chromosome 1p32, a locus associated with late-onset PD (Hicks et al., 2002). In the present study we investigated the role of FAF1 in cell death and in Parkinson’s disease (PD) pathogenesis. FAF1 levels were significantly increased in frontal cortex of PD as well as in PD cases with Alzheimer’s disease (AD) pathology compared to control cases. Changes in FAF1 expression were specific to PD-related α-synuclein pathology and nigral cell loss. In addition, PD-related insults including, mitochondrial complex I inhibition, oxidative stress, and increased α-synuclein expression specifically increased endogenous FAF1 expression in vitro. Increased FAF1 levels induced cell death and significantly potentiated toxic effects of PD-related stressors including, oxidative stress, mitochondrial complex I inhibition and proteasomal inhibition. These studies, together with previous genetic linkage studies, highlight the potential significance of FAF1 in pathogenesis of idiopathic PD.

Copyright information:

© 2008 Elsevier Inc. All rights reserved.

This is an Open Access work distributed under the terms of the Creative Commons Attribution-NonCommerical-NoDerivs 3.0 Unported License (http://creativecommons.org/licenses/by-nc-nd/3.0/).

Creative Commons License

Export to EndNote