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X. Wang, S. Zhu, M. Drozda, W. Zhang, I. G. Stavrovskaya, E. Cattaneo, R. J. Ferrante, B. S. Kristal and R. M. Friedlander, “Minocycline Inhibits Caspase-independent and -Dependent Mitochondrial Cell Death Pathways in Models of Huntington’s Disease,” Proceedings of the National Academy of Science of the United States of America, Vol. 100, No. 18, 2003, pp. 10483-10487. doi:10.1073/pnas.1832501100

has been cited by the following article:

• TITLE: Lipopolysaccharide Modified Liposomes for Amyotropic Lateral Sclerosis Therapy: Efficacy in SOD1 Mouse Model

  AUTHORS: Nicholas J. Wiley, A. B. Madhankumar, Ryan M. Mitchell, Elizabeth B. Neely, Elias Rizk, Gregory L. Douds, Zachary Simmons, James R. Connor

  KEYWORDS: Amyotrophic Lateral Sclerosis; Minocycline; Liposomes; Microglia; TLR4; Lipopolysaccharides

  JOURNAL NAME: Advances in Nanoparticles, Vol.1 No.3, November 30, 2012

  ABSTRACT: Activation of microglia is a histological feature observed in neurodegenerative diseases like ALS. The oral administration of minocycline has been demonstrated to have minimal neuroprotection ability in the animal models and is also associated with inadvertent toxicity due to non-specific oral absorption of the drug. Nonetheless, the drug itself shows promise in a number of disease models suggesting it could be effective if delivered optimally. Thus, we utilized LPS modified liposomes to target TLR4 receptor on the microglia in SOD1G93A mice and compared its efficacy with non- targeted nanoliposomes. The in vitro results indicate that targeting the TLR4 receptor on microglia significantly increases (p G93A mouse model of ALS, targeted and non-targeted minocycline treatment significantly increased (p G93A mice, the non- targeted nanovesicles significantly increased the latency to rotarod failure and both targeted and non-targeted nanovesicles significantly delayed disease endpoints.