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  P. Jafar-Nejad  

Paymaan Jafar-Nejad, Ph.D., Post-doc

Phone: 713-798-4993
Email: jafarnej@bcm.edu

Joined the lab: 2006

 
 

Education:

1993-2000   School of Medicine, Tehran University of Medical Sciences, Tehran, Iran (1993-2000)

 
     
 

Projects: Since joining Dr. Zoghbi’s lab, I have been working to understand the neuropathology of the triplet repeat disease, Spinocerebellar ataxia type 1 (SCA1), a delayed onset neurodegenerative disease, whose presenting signs reflect cerebellar dysfunction, eventually affecting multiple regions of the brain. My research has demonstrated that there is at least one modifier that exerts various effects in different brain regions. 14-3-3 epsilon haploinsufficiency can rescue the cerebellar phenotypes (but not non-cerebellar phenotypes) of the SCA1 mouse model. There might be other ATXN1 interactors that are important for the pathology outside of the cerebellum. Investigating other Ataxin1 protein interactors, their relationship with the polyQ expansion, and the pathways affected in SCA1 disease, can teach us more about the pathophysiology of SCA1. By examining over 100 ATXN1 interactors for dependence on the expansion of the polyglutamine tract, I found more than 30 interactors affected by polyglutamine tract length. Subsequent experiments using fly genetics, as well as biochemical and histological experiments, revealed that SCA1 shares certain pathological pathways with ataxia telangiectasia, Alzheimer’s disease, and amyotrophic lateral sclerosis. I am currently working to characterize these pathways more closely.

 
     
 

Selected publications:

  1. Jafar-Nejad P, Ward CS, Richman R, Orr HT, Zoghbi HY. Regional rescue of spinocerebellar ataxia type 1 phenotypes by 14-3-3? haploinsufficiency in mice underscores complex pathogenicity in neurodegeneration. Proc Natl Acad Sci USA. 2011 Feb 1;108(5):2142-7. PubMed PMID: PMC3033247.
  2. Lim J, Crespo-Barreto J, Jafar-Nejad P, Bowman AB, Richman R, Hill DE, Orr HT, Zoghbi HY. Opposing effects of polyglutamine expansion on native protein complexes contribute to SCA1. Nature. 2008 Apr 10;452(7188):713-8. PubMed PMID: PMC2377396
  3. Gatchel JR, Watase K, Thaller C, Carson JP, Jafar-Nejad P, Shaw C, Zu T, Orr HT, Zoghbi HY. The insulin-like growth factor pathway is altered in spinocerebellar ataxia type 1 and type 7. Proc Natl Acad Sci USA. 2008 Jan 29;105(4):1291-6. PubMed PMID: PMC2234131
  4. Bowman AB, Lam YC, Jafar-Nejad P, Chen HK, Richman R, Samaco RC, Fryer JD, Kahle JJ, Orr HT, Zoghbi HY. Duplication of Atxn1l suppresses SCA1 neuropathology by decreasing incorporation of polyglutamine-expanded ataxin-1 into native complexes. Nature Genetic. 2007 Mar;39(3):373-379. PubMed PMID: 17322884
  5. Lam YC, Bowman AB, Jafar-Nejad P, Lim J, Richman R, Fryer JD, Hyun ED, Duvick LA, Orr HT, Botas J, Zoghbi HY. ATAXIN-1 Interacts with the Repressor Capicua in its Native Complex to Cause SCA1 Neuropathology. Cell. 2006 Dec 29;127(7):1335-47. PubMed PMID: 17190598
  6. Jafar-Nejad P, Maricich SM, and Zoghbi HY. The Cerebellum and the Hereditary Ataxias (Chapter. 67) Swaiman’s PEDIATRIC NEUROLOGY: Principles & Practice, 5th edition, Elsevier 2010
 
     
  Hobbies or Interests:
I have been an acting member of Houston Playback Theatre since 2007. I enjoy Persian literature, playing the guitar and tar, a traditional Iranian instrument, and cooking.
 
     
     


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Last Modified: March 27, 2007