Patents by Inventor Benjamin M. Segal

Benjamin M. Segal has filed for patents to protect the following inventions. This listing includes patent applications that are pending as well as patents that have already been granted by the United States Patent and Trademark Office (USPTO).

  • Publication number: 20210113611
    Abstract: Provided herein are compositions and methods for treating neurological disorders. In particular, provided herein are neutrophils that rescue damaged neurons, methods of making such neutrophils, and methods of promoting generation of such neutrophils in vivo.
    Type: Application
    Filed: January 31, 2019
    Publication date: April 22, 2021
    Inventors: Benjamin M. Segal, Andrew Sas, Kevin Carbajal
  • Patent number: 8546538
    Abstract: Experimental autoimmune encephalomyelitis (EAE) is a Th1-mediated autoimmune disease of the central nervous system that is widely used as an animal model of multiple sclerosis (MS). In this study it was demonstrate that CXCL13, a chemokine involved in the development of secondary lymphoid tissues, is expressed in CD11c+ myeloid cells that accumulate in EAE lesions. Blockade or deficiency of CXCL13 ameliorates clinical EAE, both during acute and relapsing stages. CXCL13 deficiency did not inhibit the priming or differentiation of autoimmune effector T-cells in the periphery, but appeared to exert its effects during the effector phase of pathogenesis. These findings indicate that reagents that antagonize or inhibit CXCL13 are useful for the treatment of neuroinflammatory diseases such as MS.
    Type: Grant
    Filed: April 9, 2008
    Date of Patent: October 1, 2013
    Assignee: University of Rochester
    Inventors: Benjamin M. Segal, Ludmila Bagaeva
  • Publication number: 20110158982
    Abstract: The present invention relates to therapeutic targets for multiple sclerosis and neuroinflammatory diseases and injuries. In particular, the present invention relates to targeting MAdCAM in the treatment of such disorders.
    Type: Application
    Filed: October 4, 2010
    Publication date: June 30, 2011
    Applicant: THE REGENTS OF THE UNIVERSITY OF MICHIGAN
    Inventors: Benjamin M. Segal, Praveen Rao
  • Publication number: 20110117092
    Abstract: The present invention relates to therapeutic targets for multiple sclerosis and other inflammatory and neurological diseases. In particular, the present invention relates to altering G-CSF/G-CSFR signaling in the treatment of such disorders.
    Type: Application
    Filed: October 18, 2010
    Publication date: May 19, 2011
    Applicant: THE REGENTS OF THE UNIVERSITY OF MICHIGAN
    Inventors: Benjamin M. Segal, Praveen Rao
  • Publication number: 20080279849
    Abstract: Experimental autoimmune encephalomyelitis (EAE) is a Th1-mediated autoimmune disease of the central nervous system that is widely used as an animal model of multiple sclerosis (MS). In this study it was demonstrate that CXCL13, a chemokine involved in the development of secondary lymphoid tissues, is expressed in CD11c+ myeloid cells that accumulate in EAE lesions. Blockade or deficiency of CXCL13 ameliorates clinical EAE, both during acute and relapsing stages. CXCL13 deficiency did not inhibit the priming or differentiation of autoimmune effector T-cells in the periphery, but appeared to exert its effects during the effector phase of pathogenesis. These findings indicate that reagents that antagonize or inhibit CXCL13 are useful for the treatment of neuroinflammatory diseases such as MS.
    Type: Application
    Filed: April 9, 2008
    Publication date: November 13, 2008
    Applicant: University of Rochester
    Inventors: Benjamin M. Segal, Ludmila Bagaeva
  • Patent number: 7390884
    Abstract: Experimental autoimmune encephalomyelitis (EAE) is a Th1-mediated autoimmune disease of the central nervous system that is widely used as an animal model of multiple sclerosis (MS). In this study it was demonstrate that CXCL13, a chemokine involved in the development of secondary lymphoid tissues, is expressed in CD11c+ myeloid cells that accumulate in EAE lesions. Blockade or deficiency of CXCL13 ameliorates clinical EAE, both during acute and relapsing stages. CXCL13 deficiency did not inhibit the priming or differentiation of autoimmune effector T-cells in the periphery, but appeared to exert its effects during the effector phase of pathogenesis. These findings indicate that reagents that antagonize or inhibit CXCL13 are useful for the treatment of neuroinflammatory diseases such as MS.
    Type: Grant
    Filed: April 29, 2005
    Date of Patent: June 24, 2008
    Assignee: University of Rochester
    Inventors: Benjamin M. Segal, Ludmila Bagaeva