UCLA Neuroscience Program Ph.D. Admissions Neuroscience Faculty UCLA and Beyond  



Bruce Kagan
Neurotoxicity Caused by Channel Forming Toxins


Mailing Address:
760 westwood plaza
Phone Numbers:
310 206 2372

Selected Publications:

Quist, A., Doudevski, I., Lin, H., Azimova, R., Ng, D., Frangione, B., Kagan, B., Ghiso, J., Lal, R. Amyloid ion channels: A common structural link for protein-misfolding disease.. Proc Natl Acad Sci USA 2005; 102(30): 10427-32.
Kagan, B.L. Amyloidosis and protein folding. Science 2005; 307: 42-3.
Kagan, B.L., Azimova, R., Azimov, R. Amyloid peptide channels.. J Memb Biol 2004; 202: 1-10.
Lin, M-C., Mirzabekov, T., Kagan, B.L. Electrophysiologic Properties of Alpha Beta 25-35 channels.. Peptides 2002; 23(7): 1215-28.
Hirakura, Y., Lin, M-C., Kagan, B.L. The Channel hypothesis of Alzheimer's disease: current status. Peptides 2002; 23(7): 1311-5.
Hirakura, Y., Kagan, B.L. The channel hypothesis of amyloidosis.. Cellular and Molecular Mechanics of Toxin Action 2002; Vol. 5, (in press): .
Kagan, BL Hirakura, Y Azimov, R Azimova, R The channel hypothesis of Huntington's disease.. Brain research bulletin. . 2001; 56(3-4): 281-4.
Kagan, BL Hirakura, Y Azimov, R Azimova, R Lin, MC The channel hypothesis of Alzheimer's disease: current status.. Peptides. . 2002; 23(7): 1311-5.
Hirakura, Y Kagan, BL Pore formation by beta-2-microglobulin: a mechanism for the pathogenesis of dialysis associated amyloidosis.. Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis. . 2001; 8(2): 94-100.
Research Interest:

Bruce L. Kagan, MD., Ph.D. Dr. Kagan's research focuses on neurotoxicity caused by channel forming toxins. His laboratory examines the mechanisms by which various proteins and toxins can interact with neuronal cell membranes, triggering cell death and degeneration. Current projects are focused on the role of amyloid forming proteins (from Alzheimer's, Parkinson's, and mad cow disease)in neuronal toxicity, and testing of possible interventions to prevent channel formation or to block channels once formed and thus ameliorate the cellular destruction caused by these toxins.