Selected Publications
  • Selected from 32 peer-reviewed publications or submitted manuscripts.
  • Imam SZ, Sriram SR, Liao X, Ko HS, Savitt JM, Zhou Q, Pearson DW, Yamamoto A, Valente AJ, Andres-Mateos E, Trinkaus DB, Schools SE, Pletnikova O, Troncoso JC, Ali SF, Bains MC, Roberts JL, Kahle PJ, Dawson VL, Clark RA, Li S, Dawson TM. Inhibition of Parkin's E3 Ubiquitin Ligase Activity Through c-Abl mediated Tyrosine Phosphorylation: Implications for Parkinson's Disease. Nature Medicine (in press).
  • Imam SZ, Indig FE, Cheng WH, Saxena SP, Stevnsner T, Kufe D, Bohr VA. (2007) Cockayne syndrome protein B interacts with and is phosphorylated by c-Abl tyrosine kinase. Nucleic Acids Research (in press).
  • Wong HK, Muftuoglu M, Beck G, Imam SZ, Bohr VA, Wilson DM III. (2007) Cockayne syndrome B protein stimulates apurinic endonuclease 1 activity and protects against agents that introduce base excision repair intermediates. Nucleic Acids Research 35(12):4103-4113.
  • Imam SZ, Jankovic J, Ali SF, Skinner JT, Xie W, Conneely OM, Le WD. (2005) Nitric oxide mediates increased susceptibility to dopaminergic damage in Nurr1 heterozygous mice. FASEB J 19(11):1441-1450.
  • Imam SZ, Karahalil B, Hogue BA, Souza-Pinto NC, Bohr VA. (July 2005) Mitochondrial and nuclear DNA-repair capacity of various brain regions in mouse is altered in an age-dependent manner. Neurobiol Aging.
  • He Y, Imam SZ, Dong Z, Jankovic J, Ali SF, Appel SH, Le W. (2003) Role of nitric oxide in rotenone-induced nigro-striatal injury. J Neurochem 86(6):1338-1345.
  • Imam SZ, Ali SF. (2001) Aging increases the susceptibility to methamphetamine-induced dopaminergic neurotoxicity in rats: Correlation with peroxynitrite production and hyperthermia. J Neurochem 78(5):952-959.
  • Imam SZ, Newport GD, Itzhak Y, Cadet JL, Islam F, Slikker W, Ali SF. (2001) Peroxynitrite plays a role in methamphetamine-induced dopaminergic neurotoxicity: Evidence from mice lacking neuronal nitric oxide synthase gene or overexpressing copper-zinc superoxide dismutase. J Neurochem 76(3):745-749.
  • Imam SZ, Islam F, Itzhak Y, Slikker W, Ali SF. (2000) Prevention of dopaminergic neurotoxicity by targeting nitric oxide and peroxynitrite: Implications for the prevention of methamphetamine-induced neurotoxic damage. Ann NY Acad Sci 914:157-171.
  • Imam SZ, Ali SF. (2000) Selenium, an antioxidant, attenuates methamphetamine-induced dopaminergic toxicity and peroxynitrite generation. Brain Res 855(1):186-191.
  • Imam SZ, Crow JP, Newport GD, Islam F, Slikker W, Ali SF. (1999) Methamphetamine generates peroxynitrite and produces dopaminergic neurotoxicity in mice: Protective effects of peroxynitrite decomposition catalyst. Brain Res 837(1-2):15-21.
  • Yu X, Imam SZ, Newport GD, Slikker W, Ali SF. (1999) Ibogaine blocked methamphetamine-induced hyperthermia and induction of heat shock protein in mice. Brain Res 823(1-2):213-216.
  • Imam SZ, Newport GD, Islam F, Slikker W, Ali SF. (1999) Selenium, an antioxidant, protects against methamphetamine-induced dopaminergic neurotoxicity. Brain Res 818(2):575-578.
Syed Imam

Syed Imam

Assistant Professor of Medicine & Pharmacology
Ph.D., Hamdard University (India) & US FDA/NCTR (Jefferson, AR)

Office: 210-567-5338



Parkinson's disease, Alzheimer's disease, Neurodegeneration, Cell Signaling, Oxidative Stress, Parkin, Tyrosine Kinases


Research Summary

The main research goal of my laboratory is to understand the molecular basis of neurodegeneration, which can be implicated to develop therapeutic trials for neurodegenerative diseases. The broad areas of investigation in my lab include the study of the molecular mechanisms of neuronal cell death, novel cell death and cell survival pathways and their correlation with the molecular basis of Parkinson's disease (PD), α-synucleinopathies and related neurodegenerative disorders. We strive to identify regulatable targets that can be manipulated by chemical or genetic means for pharmaceutical and therapeutic intervention.


Presently, my laboratory is focused on role of signaling kinases in the regulation of various components of PD as a therapeutic target in animal models and in PD patients. Our novel finding that oxidative stress sensitive tyrosine kinase renders parkin, an E3 ubiquitin ligase, non-functional has opened up various new avenues to understand progression of nigro-striatal degeneration during the pathogenesis of PD. We are investigating the role of cell signaling regulation of α-synuclein and LRRK2 in the pathogenesis of PD. Furthermore, we have ongoing pre-clinical studies on the role of kinase inhibitors as a potential therapeutic approach in slowing down the progression of PD.


In addition, we are working to develop projects on molecular signaling mechanisms during progression of AD. Furthermore, my laboratory has a very strong background in the oxidative-stress mediated neurotoxicity induced by substituted amphetamines as well as in DNA damage and repair in aging brain. My laboratory has set-up extensive collaborations with various PD research and clinical centers in USA and Europe that include Morris Udall Center of Excellence for PD Research at Johns Hopkins School of Medicine, Department of Neurology at UCSD, Hertie Institute of Clinical Brain Research at University of Tubingen, Germany and Brain Mind Institute of Swiss Federal Institute of Technology, Switzerland.


Unique technical and clinical research capabilities/instrumentation in my laboratory include Gene and Protein Interaction, Cell-Signaling Studies, Biochemical and Immunochemical analysis, HPLC analysis of neurochemicals and pro-oxidants, Gene-silencing and overexpression using plasmid, lenti- and retro-viral vectors, protein purification, kinomics, analysis of proteome and transciptome, primary and permanent neuronal cultures, animal modeling of neurodegenerative disorders, analysis of post-mortem human brain samples. Immunoprecipitation, gene-transfection, Western blots, etc.