Borrelia Neurotoxin References
1.) “We have identified and cloned a gene of B. burgdorferi which encodes a protein that is a neurotoxin.” A Novel Toxin (Bb Tox 1) of Borrelia burgdorferi. Mark J. Cartwright, Ph.D.*, Suzanne E. Martin, Ph.D. and Sam T. Donta, M.D. Boston University Medical Center, 12th Annual International Conference on Lyme Borreliosis and Other Tick-borne Disorders: Chronic Lyme Disease: Basic Science and Clinical Approaches, 1999. http://www.lyme.org/conferences/99_abstract.html
2.) “Neurotoxin, produced by B. burgdorferi Bbtox1 was identified. Encephalopathy signs in Lyme borreliosis could be result of releasing toxico-metabolic products, ability of spirochetes to pass the blood-brain barrier as well as, effect of lymphocytes migration. Active invasion of brain endothelium as ability to adherence to endothelial wall could be the source of focused or disseminated inflammation of brain vessels. Endothelial cells, toxic products of granulocytes, monocytes, macrophages as well as phagocytosis counterpart in pathogenesis. Induced cytokines are connected with activation subsets of T lymphocytes involved in inflammatory response. Cytokines produced by Th1 as cytotoxic CD8 accompany the disease.” Przegl Epidemiol. 2002;56 Suppl 1:57-67. [New aspects of the pathogenesis of lyme disease]. Zajkowska JM1, Hermanowska-Szpakowicz T. http://www.ncbi.nlm.nih.gov/pubmed/12194230
3.) “Numerous reports indicate that lipid or protein associated carbohydrates are essential for infection of cells by various viruses, bacteria, or bacterial toxins, some of which affect the nervous system. Examples of such pathogens include tetanus and botulinum neurotoxin, Shiga and Shiga-like toxins, Borrelia burgdorferi, Mycobacterium leprae, and human immunodeficiency virus.” CNS Neurol Disord Drug Targets. 2006 Aug;5(4):381-9. Glycoconjugates: roles in neural diseases caused by exogenous pathogens. Schengrund CL. The Department of Biochemistry and Molecular Biology, The Pennsylvania State University College of Medicine, Hershey, 17033, USA. http://www.ncbi.nlm.nih.gov/pubmed/16918390
4.) “Intoxication by the zinc protease botulinus neurotoxin A (BoNT-A) results from cleavage of a single Q-R bond in the neuronal protein SNAP-25, which disables the docking mechanism required for neurotransmitter release.”Hayden J, Pires J, Roy S et al.. Discovery and design of novel inhibitors of botulinus neurotoxin A: targeted "hinge" peptide libraries. J Appl Toxicol. 2003;23:1-7. http://www.ncbi.nlm.nih.gov/pubmed/?term=Discovery+and+design+of+novel+inhibitors+of+botulinus+neurotoxin
5.) “Taken together, these findings indicate that B. burgdorferi is not directly toxic to SY cells; rather, these cells become distressed and die in the inflammatory surroundings generated by microglia through a bystander effect.” Myers TA, Kaushal D, Philipp MT (2009) Microglia Are Mediators of Borrelia burgdorferi–Induced Apoptosis in SH-SY5Y Neuronal Cells. PLoS Pathog 5(11): e1000659. doi:10.1371/journal.ppat.1000659
http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1000659