Immunotherapy Clinical Trial

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David H. Cribbs - One of the best experts on this subject based on the ideXlab platform.

  • prototype alzheimer s disease vaccine using the immunodominant b cell epitope from β amyloid and promiscuous t cell epitope pan hla dr binding peptide
    Journal of Immunology, 2005
    Co-Authors: Michael G. Agadjanyan, Anahit Ghochikyan, Irina Petrushina, Vitaly Vasilevko, Nina Movsesyan, Mikayel Mkrtichyan, Tommy Saing, David H. Cribbs
    Abstract:

    Immunization of amyloid precursor protein transgenic mice with fibrillar β-amyloid (Aβ) prevents Alzheimer’s disease (AD)-like neuropathology. The first Immunotherapy Clinical Trial used fibrillar Aβ, containing the B and T cell self epitopes of Aβ, as the immunogen formulated with QS21 as the adjuvant in the vaccine. Unfortunately, the Clinical Trial was halted during the phase II stage when 6% of the participants developed meningoencephalitis. The cause of the meningoencephalitis in the patients that received the vaccine has not been definitively determined; however, analysis of two case reports from the AN-1792 vaccine Trial suggest that the meningoencephalitis may have been caused by a T cell-mediated autoimmune response, whereas production of anti-Aβ Abs may have been therapeutic to the AD patients. Therefore, to reduce the risk of an adverse T cell-mediated immune response to Aβ Immunotherapy we have designed a prototype epitope vaccine that contains the immunodominant B cell epitope of Aβ in tandem with the synthetic universal Th cell pan HLA DR epitope, pan HLA DR-binding peptide (PADRE). Importantly, the PADRE-Aβ1–15 sequence lacks the T cell epitope of Aβ. Immunization of BALB/c mice with the PADRE-Aβ1–15 epitope vaccine produced high titers of anti-Aβ Abs. Splenocytes from immunized mice showed robust T cell stimulation in response to peptides containing PADRE. However, splenocytes from immunized mice were not reactivated by the Aβ peptide. New preClinical Trials in amyloid precursor protein transgenic mouse models may help to develop novel immunogen-adjuvant configurations with the potential to avoid the adverse events that occurred in the first Clinical Trial.

  • prototype alzheimer s disease vaccine using the immunodominant b cell epitope from β amyloid and promiscuous t cell epitope pan hla dr binding peptide
    Journal of Immunology, 2005
    Co-Authors: Michael G. Agadjanyan, Anahit Ghochikyan, Irina Petrushina, Vitaly Vasilevko, Nina Movsesyan, Mikayel Mkrtichyan, Tommy Saing, David H. Cribbs
    Abstract:

    Immunization of amyloid precursor protein transgenic mice with fibrillar beta-amyloid (Abeta) prevents Alzheimer's disease (AD)-like neuropathology. The first Immunotherapy Clinical Trial used fibrillar Abeta, containing the B and T cell self epitopes of Abeta, as the immunogen formulated with QS21 as the adjuvant in the vaccine. Unfortunately, the Clinical Trial was halted during the phase II stage when 6% of the participants developed meningoencephalitis. The cause of the meningoencephalitis in the patients that received the vaccine has not been definitively determined; however, analysis of two case reports from the AN-1792 vaccine Trial suggest that the meningoencephalitis may have been caused by a T cell-mediated autoimmune response, whereas production of anti-Abeta Abs may have been therapeutic to the AD patients. Therefore, to reduce the risk of an adverse T cell-mediated immune response to Abeta Immunotherapy we have designed a prototype epitope vaccine that contains the immunodominant B cell epitope of Abeta in tandem with the synthetic universal Th cell pan HLA DR epitope, pan HLA DR-binding peptide (PADRE). Importantly, the PADRE-Abeta(1-15) sequence lacks the T cell epitope of Abeta. Immunization of BALB/c mice with the PADRE-Abeta(1-15) epitope vaccine produced high titers of anti-Abeta Abs. Splenocytes from immunized mice showed robust T cell stimulation in response to peptides containing PADRE. However, splenocytes from immunized mice were not reactivated by the Abeta peptide. New preClinical Trials in amyloid precursor protein transgenic mouse models may help to develop novel immunogen-adjuvant configurations with the potential to avoid the adverse events that occurred in the first Clinical Trial.

  • Prototype Alzheimer’s Disease Vaccine Using the Immunodominant B Cell Epitope from β-Amyloid and Promiscuous T Cell Epitope Pan HLA DR-Binding Peptide
    Journal of Immunology, 2005
    Co-Authors: Michael G. Agadjanyan, Anahit Ghochikyan, Irina Petrushina, Vitaly Vasilevko, Nina Movsesyan, Mikayel Mkrtichyan, Tommy Saing, David H. Cribbs
    Abstract:

    Immunization of amyloid precursor protein transgenic mice with fibrillar β-amyloid (Aβ) prevents Alzheimer’s disease (AD)-like neuropathology. The first Immunotherapy Clinical Trial used fibrillar Aβ, containing the B and T cell self epitopes of Aβ, as the immunogen formulated with QS21 as the adjuvant in the vaccine. Unfortunately, the Clinical Trial was halted during the phase II stage when 6% of the participants developed meningoencephalitis. The cause of the meningoencephalitis in the patients that received the vaccine has not been definitively determined; however, analysis of two case reports from the AN-1792 vaccine Trial suggest that the meningoencephalitis may have been caused by a T cell-mediated autoimmune response, whereas production of anti-Aβ Abs may have been therapeutic to the AD patients. Therefore, to reduce the risk of an adverse T cell-mediated immune response to Aβ Immunotherapy we have designed a prototype epitope vaccine that contains the immunodominant B cell epitope of Aβ in tandem with the synthetic universal Th cell pan HLA DR epitope, pan HLA DR-binding peptide (PADRE). Importantly, the PADRE-Aβ1–15 sequence lacks the T cell epitope of Aβ. Immunization of BALB/c mice with the PADRE-Aβ1–15 epitope vaccine produced high titers of anti-Aβ Abs. Splenocytes from immunized mice showed robust T cell stimulation in response to peptides containing PADRE. However, splenocytes from immunized mice were not reactivated by the Aβ peptide. New preClinical Trials in amyloid precursor protein transgenic mouse models may help to develop novel immunogen-adjuvant configurations with the potential to avoid the adverse events that occurred in the first Clinical Trial.

Michael G. Agadjanyan - One of the best experts on this subject based on the ideXlab platform.

  • Prototype Alzheimer’s Disease Vaccine Using the
    2015
    Co-Authors: Promiscuous T Cell, Michael G. Agadjanyan, Anahit Ghochikyan, Irina Petrushina, Vitaly Vasilevko, Nina Movsesyan, Mikayel Mkrtichyan, Epitope Pan, Hla Dr-binding Peptide, Tommy Saing
    Abstract:

    Immunization of amyloid precursor protein transgenic mice with fibrillar -amyloid (A) prevents Alzheimer’s disease (AD)-like neuropathology. The first Immunotherapy Clinical Trial used fibrillar A, containing the B and T cell self epitopes of A, as the immunogen formulated with QS21 as the adjuvant in the vaccine. Unfortunately, the Clinical Trial was halted during the phase II stage when 6 % of the participants developed meningoencephalitis. The cause of the meningoencephalitis in the patients that received the vaccine has not been definitively determined; however, analysis of two case reports from the AN-1792 vaccine Trial suggest that the meningoencephalitis may have been caused by a T cell-mediated autoimmune response, whereas production of anti-A Abs may have been therapeutic to the AD patients. Therefore, to reduce the risk of an adverse T cell-mediated immune response to A Immunotherapy we have designed a prototype epitope vaccine that contains the immunodominant B cell epitope of A in tandem with the synthetic universal Th cell pan HLA DR epitope, pan HLA DR-binding peptide (PADRE). Importantly, the PADRE-A1–15 sequence lacks the T cell epitope of A. Immunization of BALB/c mice with the PADRE-A1–15 epitope vaccine produced high titers of anti-A Abs. Splenocytes from immunized mice showed robust T cell stimulation in response to peptides containing PADRE. However, splenocytes from immunized mice were not reactivated by the A peptide. New preClinical Trials in amyloid precursor protein transgenic mouse models may help to develop novel immunogen-adjuvant configurations with the potential to avoid the adverse events that occurred in the first Clinical Trial. The Journal of Immunology, 2005, 174: 1580–1586. A lzheimer’s disease (AD)4 is the most common form ofdementia in the elderly and is characterized by a pro-gressive loss of memory and a general cognitive decline

  • prototype alzheimer s disease vaccine using the immunodominant b cell epitope from β amyloid and promiscuous t cell epitope pan hla dr binding peptide
    Journal of Immunology, 2005
    Co-Authors: Michael G. Agadjanyan, Anahit Ghochikyan, Irina Petrushina, Vitaly Vasilevko, Nina Movsesyan, Mikayel Mkrtichyan, Tommy Saing, David H. Cribbs
    Abstract:

    Immunization of amyloid precursor protein transgenic mice with fibrillar β-amyloid (Aβ) prevents Alzheimer’s disease (AD)-like neuropathology. The first Immunotherapy Clinical Trial used fibrillar Aβ, containing the B and T cell self epitopes of Aβ, as the immunogen formulated with QS21 as the adjuvant in the vaccine. Unfortunately, the Clinical Trial was halted during the phase II stage when 6% of the participants developed meningoencephalitis. The cause of the meningoencephalitis in the patients that received the vaccine has not been definitively determined; however, analysis of two case reports from the AN-1792 vaccine Trial suggest that the meningoencephalitis may have been caused by a T cell-mediated autoimmune response, whereas production of anti-Aβ Abs may have been therapeutic to the AD patients. Therefore, to reduce the risk of an adverse T cell-mediated immune response to Aβ Immunotherapy we have designed a prototype epitope vaccine that contains the immunodominant B cell epitope of Aβ in tandem with the synthetic universal Th cell pan HLA DR epitope, pan HLA DR-binding peptide (PADRE). Importantly, the PADRE-Aβ1–15 sequence lacks the T cell epitope of Aβ. Immunization of BALB/c mice with the PADRE-Aβ1–15 epitope vaccine produced high titers of anti-Aβ Abs. Splenocytes from immunized mice showed robust T cell stimulation in response to peptides containing PADRE. However, splenocytes from immunized mice were not reactivated by the Aβ peptide. New preClinical Trials in amyloid precursor protein transgenic mouse models may help to develop novel immunogen-adjuvant configurations with the potential to avoid the adverse events that occurred in the first Clinical Trial.

  • prototype alzheimer s disease vaccine using the immunodominant b cell epitope from β amyloid and promiscuous t cell epitope pan hla dr binding peptide
    Journal of Immunology, 2005
    Co-Authors: Michael G. Agadjanyan, Anahit Ghochikyan, Irina Petrushina, Vitaly Vasilevko, Nina Movsesyan, Mikayel Mkrtichyan, Tommy Saing, David H. Cribbs
    Abstract:

    Immunization of amyloid precursor protein transgenic mice with fibrillar beta-amyloid (Abeta) prevents Alzheimer's disease (AD)-like neuropathology. The first Immunotherapy Clinical Trial used fibrillar Abeta, containing the B and T cell self epitopes of Abeta, as the immunogen formulated with QS21 as the adjuvant in the vaccine. Unfortunately, the Clinical Trial was halted during the phase II stage when 6% of the participants developed meningoencephalitis. The cause of the meningoencephalitis in the patients that received the vaccine has not been definitively determined; however, analysis of two case reports from the AN-1792 vaccine Trial suggest that the meningoencephalitis may have been caused by a T cell-mediated autoimmune response, whereas production of anti-Abeta Abs may have been therapeutic to the AD patients. Therefore, to reduce the risk of an adverse T cell-mediated immune response to Abeta Immunotherapy we have designed a prototype epitope vaccine that contains the immunodominant B cell epitope of Abeta in tandem with the synthetic universal Th cell pan HLA DR epitope, pan HLA DR-binding peptide (PADRE). Importantly, the PADRE-Abeta(1-15) sequence lacks the T cell epitope of Abeta. Immunization of BALB/c mice with the PADRE-Abeta(1-15) epitope vaccine produced high titers of anti-Abeta Abs. Splenocytes from immunized mice showed robust T cell stimulation in response to peptides containing PADRE. However, splenocytes from immunized mice were not reactivated by the Abeta peptide. New preClinical Trials in amyloid precursor protein transgenic mouse models may help to develop novel immunogen-adjuvant configurations with the potential to avoid the adverse events that occurred in the first Clinical Trial.

  • Prototype Alzheimer’s Disease Vaccine Using the Immunodominant B Cell Epitope from β-Amyloid and Promiscuous T Cell Epitope Pan HLA DR-Binding Peptide
    Journal of Immunology, 2005
    Co-Authors: Michael G. Agadjanyan, Anahit Ghochikyan, Irina Petrushina, Vitaly Vasilevko, Nina Movsesyan, Mikayel Mkrtichyan, Tommy Saing, David H. Cribbs
    Abstract:

    Immunization of amyloid precursor protein transgenic mice with fibrillar β-amyloid (Aβ) prevents Alzheimer’s disease (AD)-like neuropathology. The first Immunotherapy Clinical Trial used fibrillar Aβ, containing the B and T cell self epitopes of Aβ, as the immunogen formulated with QS21 as the adjuvant in the vaccine. Unfortunately, the Clinical Trial was halted during the phase II stage when 6% of the participants developed meningoencephalitis. The cause of the meningoencephalitis in the patients that received the vaccine has not been definitively determined; however, analysis of two case reports from the AN-1792 vaccine Trial suggest that the meningoencephalitis may have been caused by a T cell-mediated autoimmune response, whereas production of anti-Aβ Abs may have been therapeutic to the AD patients. Therefore, to reduce the risk of an adverse T cell-mediated immune response to Aβ Immunotherapy we have designed a prototype epitope vaccine that contains the immunodominant B cell epitope of Aβ in tandem with the synthetic universal Th cell pan HLA DR epitope, pan HLA DR-binding peptide (PADRE). Importantly, the PADRE-Aβ1–15 sequence lacks the T cell epitope of Aβ. Immunization of BALB/c mice with the PADRE-Aβ1–15 epitope vaccine produced high titers of anti-Aβ Abs. Splenocytes from immunized mice showed robust T cell stimulation in response to peptides containing PADRE. However, splenocytes from immunized mice were not reactivated by the Aβ peptide. New preClinical Trials in amyloid precursor protein transgenic mouse models may help to develop novel immunogen-adjuvant configurations with the potential to avoid the adverse events that occurred in the first Clinical Trial.

Tommy Saing - One of the best experts on this subject based on the ideXlab platform.

  • Prototype Alzheimer’s Disease Vaccine Using the
    2015
    Co-Authors: Promiscuous T Cell, Michael G. Agadjanyan, Anahit Ghochikyan, Irina Petrushina, Vitaly Vasilevko, Nina Movsesyan, Mikayel Mkrtichyan, Epitope Pan, Hla Dr-binding Peptide, Tommy Saing
    Abstract:

    Immunization of amyloid precursor protein transgenic mice with fibrillar -amyloid (A) prevents Alzheimer’s disease (AD)-like neuropathology. The first Immunotherapy Clinical Trial used fibrillar A, containing the B and T cell self epitopes of A, as the immunogen formulated with QS21 as the adjuvant in the vaccine. Unfortunately, the Clinical Trial was halted during the phase II stage when 6 % of the participants developed meningoencephalitis. The cause of the meningoencephalitis in the patients that received the vaccine has not been definitively determined; however, analysis of two case reports from the AN-1792 vaccine Trial suggest that the meningoencephalitis may have been caused by a T cell-mediated autoimmune response, whereas production of anti-A Abs may have been therapeutic to the AD patients. Therefore, to reduce the risk of an adverse T cell-mediated immune response to A Immunotherapy we have designed a prototype epitope vaccine that contains the immunodominant B cell epitope of A in tandem with the synthetic universal Th cell pan HLA DR epitope, pan HLA DR-binding peptide (PADRE). Importantly, the PADRE-A1–15 sequence lacks the T cell epitope of A. Immunization of BALB/c mice with the PADRE-A1–15 epitope vaccine produced high titers of anti-A Abs. Splenocytes from immunized mice showed robust T cell stimulation in response to peptides containing PADRE. However, splenocytes from immunized mice were not reactivated by the A peptide. New preClinical Trials in amyloid precursor protein transgenic mouse models may help to develop novel immunogen-adjuvant configurations with the potential to avoid the adverse events that occurred in the first Clinical Trial. The Journal of Immunology, 2005, 174: 1580–1586. A lzheimer’s disease (AD)4 is the most common form ofdementia in the elderly and is characterized by a pro-gressive loss of memory and a general cognitive decline

  • prototype alzheimer s disease vaccine using the immunodominant b cell epitope from β amyloid and promiscuous t cell epitope pan hla dr binding peptide
    Journal of Immunology, 2005
    Co-Authors: Michael G. Agadjanyan, Anahit Ghochikyan, Irina Petrushina, Vitaly Vasilevko, Nina Movsesyan, Mikayel Mkrtichyan, Tommy Saing, David H. Cribbs
    Abstract:

    Immunization of amyloid precursor protein transgenic mice with fibrillar β-amyloid (Aβ) prevents Alzheimer’s disease (AD)-like neuropathology. The first Immunotherapy Clinical Trial used fibrillar Aβ, containing the B and T cell self epitopes of Aβ, as the immunogen formulated with QS21 as the adjuvant in the vaccine. Unfortunately, the Clinical Trial was halted during the phase II stage when 6% of the participants developed meningoencephalitis. The cause of the meningoencephalitis in the patients that received the vaccine has not been definitively determined; however, analysis of two case reports from the AN-1792 vaccine Trial suggest that the meningoencephalitis may have been caused by a T cell-mediated autoimmune response, whereas production of anti-Aβ Abs may have been therapeutic to the AD patients. Therefore, to reduce the risk of an adverse T cell-mediated immune response to Aβ Immunotherapy we have designed a prototype epitope vaccine that contains the immunodominant B cell epitope of Aβ in tandem with the synthetic universal Th cell pan HLA DR epitope, pan HLA DR-binding peptide (PADRE). Importantly, the PADRE-Aβ1–15 sequence lacks the T cell epitope of Aβ. Immunization of BALB/c mice with the PADRE-Aβ1–15 epitope vaccine produced high titers of anti-Aβ Abs. Splenocytes from immunized mice showed robust T cell stimulation in response to peptides containing PADRE. However, splenocytes from immunized mice were not reactivated by the Aβ peptide. New preClinical Trials in amyloid precursor protein transgenic mouse models may help to develop novel immunogen-adjuvant configurations with the potential to avoid the adverse events that occurred in the first Clinical Trial.

  • prototype alzheimer s disease vaccine using the immunodominant b cell epitope from β amyloid and promiscuous t cell epitope pan hla dr binding peptide
    Journal of Immunology, 2005
    Co-Authors: Michael G. Agadjanyan, Anahit Ghochikyan, Irina Petrushina, Vitaly Vasilevko, Nina Movsesyan, Mikayel Mkrtichyan, Tommy Saing, David H. Cribbs
    Abstract:

    Immunization of amyloid precursor protein transgenic mice with fibrillar beta-amyloid (Abeta) prevents Alzheimer's disease (AD)-like neuropathology. The first Immunotherapy Clinical Trial used fibrillar Abeta, containing the B and T cell self epitopes of Abeta, as the immunogen formulated with QS21 as the adjuvant in the vaccine. Unfortunately, the Clinical Trial was halted during the phase II stage when 6% of the participants developed meningoencephalitis. The cause of the meningoencephalitis in the patients that received the vaccine has not been definitively determined; however, analysis of two case reports from the AN-1792 vaccine Trial suggest that the meningoencephalitis may have been caused by a T cell-mediated autoimmune response, whereas production of anti-Abeta Abs may have been therapeutic to the AD patients. Therefore, to reduce the risk of an adverse T cell-mediated immune response to Abeta Immunotherapy we have designed a prototype epitope vaccine that contains the immunodominant B cell epitope of Abeta in tandem with the synthetic universal Th cell pan HLA DR epitope, pan HLA DR-binding peptide (PADRE). Importantly, the PADRE-Abeta(1-15) sequence lacks the T cell epitope of Abeta. Immunization of BALB/c mice with the PADRE-Abeta(1-15) epitope vaccine produced high titers of anti-Abeta Abs. Splenocytes from immunized mice showed robust T cell stimulation in response to peptides containing PADRE. However, splenocytes from immunized mice were not reactivated by the Abeta peptide. New preClinical Trials in amyloid precursor protein transgenic mouse models may help to develop novel immunogen-adjuvant configurations with the potential to avoid the adverse events that occurred in the first Clinical Trial.

  • Prototype Alzheimer’s Disease Vaccine Using the Immunodominant B Cell Epitope from β-Amyloid and Promiscuous T Cell Epitope Pan HLA DR-Binding Peptide
    Journal of Immunology, 2005
    Co-Authors: Michael G. Agadjanyan, Anahit Ghochikyan, Irina Petrushina, Vitaly Vasilevko, Nina Movsesyan, Mikayel Mkrtichyan, Tommy Saing, David H. Cribbs
    Abstract:

    Immunization of amyloid precursor protein transgenic mice with fibrillar β-amyloid (Aβ) prevents Alzheimer’s disease (AD)-like neuropathology. The first Immunotherapy Clinical Trial used fibrillar Aβ, containing the B and T cell self epitopes of Aβ, as the immunogen formulated with QS21 as the adjuvant in the vaccine. Unfortunately, the Clinical Trial was halted during the phase II stage when 6% of the participants developed meningoencephalitis. The cause of the meningoencephalitis in the patients that received the vaccine has not been definitively determined; however, analysis of two case reports from the AN-1792 vaccine Trial suggest that the meningoencephalitis may have been caused by a T cell-mediated autoimmune response, whereas production of anti-Aβ Abs may have been therapeutic to the AD patients. Therefore, to reduce the risk of an adverse T cell-mediated immune response to Aβ Immunotherapy we have designed a prototype epitope vaccine that contains the immunodominant B cell epitope of Aβ in tandem with the synthetic universal Th cell pan HLA DR epitope, pan HLA DR-binding peptide (PADRE). Importantly, the PADRE-Aβ1–15 sequence lacks the T cell epitope of Aβ. Immunization of BALB/c mice with the PADRE-Aβ1–15 epitope vaccine produced high titers of anti-Aβ Abs. Splenocytes from immunized mice showed robust T cell stimulation in response to peptides containing PADRE. However, splenocytes from immunized mice were not reactivated by the Aβ peptide. New preClinical Trials in amyloid precursor protein transgenic mouse models may help to develop novel immunogen-adjuvant configurations with the potential to avoid the adverse events that occurred in the first Clinical Trial.

Mikayel Mkrtichyan - One of the best experts on this subject based on the ideXlab platform.

  • Prototype Alzheimer’s Disease Vaccine Using the
    2015
    Co-Authors: Promiscuous T Cell, Michael G. Agadjanyan, Anahit Ghochikyan, Irina Petrushina, Vitaly Vasilevko, Nina Movsesyan, Mikayel Mkrtichyan, Epitope Pan, Hla Dr-binding Peptide, Tommy Saing
    Abstract:

    Immunization of amyloid precursor protein transgenic mice with fibrillar -amyloid (A) prevents Alzheimer’s disease (AD)-like neuropathology. The first Immunotherapy Clinical Trial used fibrillar A, containing the B and T cell self epitopes of A, as the immunogen formulated with QS21 as the adjuvant in the vaccine. Unfortunately, the Clinical Trial was halted during the phase II stage when 6 % of the participants developed meningoencephalitis. The cause of the meningoencephalitis in the patients that received the vaccine has not been definitively determined; however, analysis of two case reports from the AN-1792 vaccine Trial suggest that the meningoencephalitis may have been caused by a T cell-mediated autoimmune response, whereas production of anti-A Abs may have been therapeutic to the AD patients. Therefore, to reduce the risk of an adverse T cell-mediated immune response to A Immunotherapy we have designed a prototype epitope vaccine that contains the immunodominant B cell epitope of A in tandem with the synthetic universal Th cell pan HLA DR epitope, pan HLA DR-binding peptide (PADRE). Importantly, the PADRE-A1–15 sequence lacks the T cell epitope of A. Immunization of BALB/c mice with the PADRE-A1–15 epitope vaccine produced high titers of anti-A Abs. Splenocytes from immunized mice showed robust T cell stimulation in response to peptides containing PADRE. However, splenocytes from immunized mice were not reactivated by the A peptide. New preClinical Trials in amyloid precursor protein transgenic mouse models may help to develop novel immunogen-adjuvant configurations with the potential to avoid the adverse events that occurred in the first Clinical Trial. The Journal of Immunology, 2005, 174: 1580–1586. A lzheimer’s disease (AD)4 is the most common form ofdementia in the elderly and is characterized by a pro-gressive loss of memory and a general cognitive decline

  • prototype alzheimer s disease vaccine using the immunodominant b cell epitope from β amyloid and promiscuous t cell epitope pan hla dr binding peptide
    Journal of Immunology, 2005
    Co-Authors: Michael G. Agadjanyan, Anahit Ghochikyan, Irina Petrushina, Vitaly Vasilevko, Nina Movsesyan, Mikayel Mkrtichyan, Tommy Saing, David H. Cribbs
    Abstract:

    Immunization of amyloid precursor protein transgenic mice with fibrillar β-amyloid (Aβ) prevents Alzheimer’s disease (AD)-like neuropathology. The first Immunotherapy Clinical Trial used fibrillar Aβ, containing the B and T cell self epitopes of Aβ, as the immunogen formulated with QS21 as the adjuvant in the vaccine. Unfortunately, the Clinical Trial was halted during the phase II stage when 6% of the participants developed meningoencephalitis. The cause of the meningoencephalitis in the patients that received the vaccine has not been definitively determined; however, analysis of two case reports from the AN-1792 vaccine Trial suggest that the meningoencephalitis may have been caused by a T cell-mediated autoimmune response, whereas production of anti-Aβ Abs may have been therapeutic to the AD patients. Therefore, to reduce the risk of an adverse T cell-mediated immune response to Aβ Immunotherapy we have designed a prototype epitope vaccine that contains the immunodominant B cell epitope of Aβ in tandem with the synthetic universal Th cell pan HLA DR epitope, pan HLA DR-binding peptide (PADRE). Importantly, the PADRE-Aβ1–15 sequence lacks the T cell epitope of Aβ. Immunization of BALB/c mice with the PADRE-Aβ1–15 epitope vaccine produced high titers of anti-Aβ Abs. Splenocytes from immunized mice showed robust T cell stimulation in response to peptides containing PADRE. However, splenocytes from immunized mice were not reactivated by the Aβ peptide. New preClinical Trials in amyloid precursor protein transgenic mouse models may help to develop novel immunogen-adjuvant configurations with the potential to avoid the adverse events that occurred in the first Clinical Trial.

  • prototype alzheimer s disease vaccine using the immunodominant b cell epitope from β amyloid and promiscuous t cell epitope pan hla dr binding peptide
    Journal of Immunology, 2005
    Co-Authors: Michael G. Agadjanyan, Anahit Ghochikyan, Irina Petrushina, Vitaly Vasilevko, Nina Movsesyan, Mikayel Mkrtichyan, Tommy Saing, David H. Cribbs
    Abstract:

    Immunization of amyloid precursor protein transgenic mice with fibrillar beta-amyloid (Abeta) prevents Alzheimer's disease (AD)-like neuropathology. The first Immunotherapy Clinical Trial used fibrillar Abeta, containing the B and T cell self epitopes of Abeta, as the immunogen formulated with QS21 as the adjuvant in the vaccine. Unfortunately, the Clinical Trial was halted during the phase II stage when 6% of the participants developed meningoencephalitis. The cause of the meningoencephalitis in the patients that received the vaccine has not been definitively determined; however, analysis of two case reports from the AN-1792 vaccine Trial suggest that the meningoencephalitis may have been caused by a T cell-mediated autoimmune response, whereas production of anti-Abeta Abs may have been therapeutic to the AD patients. Therefore, to reduce the risk of an adverse T cell-mediated immune response to Abeta Immunotherapy we have designed a prototype epitope vaccine that contains the immunodominant B cell epitope of Abeta in tandem with the synthetic universal Th cell pan HLA DR epitope, pan HLA DR-binding peptide (PADRE). Importantly, the PADRE-Abeta(1-15) sequence lacks the T cell epitope of Abeta. Immunization of BALB/c mice with the PADRE-Abeta(1-15) epitope vaccine produced high titers of anti-Abeta Abs. Splenocytes from immunized mice showed robust T cell stimulation in response to peptides containing PADRE. However, splenocytes from immunized mice were not reactivated by the Abeta peptide. New preClinical Trials in amyloid precursor protein transgenic mouse models may help to develop novel immunogen-adjuvant configurations with the potential to avoid the adverse events that occurred in the first Clinical Trial.

  • Prototype Alzheimer’s Disease Vaccine Using the Immunodominant B Cell Epitope from β-Amyloid and Promiscuous T Cell Epitope Pan HLA DR-Binding Peptide
    Journal of Immunology, 2005
    Co-Authors: Michael G. Agadjanyan, Anahit Ghochikyan, Irina Petrushina, Vitaly Vasilevko, Nina Movsesyan, Mikayel Mkrtichyan, Tommy Saing, David H. Cribbs
    Abstract:

    Immunization of amyloid precursor protein transgenic mice with fibrillar β-amyloid (Aβ) prevents Alzheimer’s disease (AD)-like neuropathology. The first Immunotherapy Clinical Trial used fibrillar Aβ, containing the B and T cell self epitopes of Aβ, as the immunogen formulated with QS21 as the adjuvant in the vaccine. Unfortunately, the Clinical Trial was halted during the phase II stage when 6% of the participants developed meningoencephalitis. The cause of the meningoencephalitis in the patients that received the vaccine has not been definitively determined; however, analysis of two case reports from the AN-1792 vaccine Trial suggest that the meningoencephalitis may have been caused by a T cell-mediated autoimmune response, whereas production of anti-Aβ Abs may have been therapeutic to the AD patients. Therefore, to reduce the risk of an adverse T cell-mediated immune response to Aβ Immunotherapy we have designed a prototype epitope vaccine that contains the immunodominant B cell epitope of Aβ in tandem with the synthetic universal Th cell pan HLA DR epitope, pan HLA DR-binding peptide (PADRE). Importantly, the PADRE-Aβ1–15 sequence lacks the T cell epitope of Aβ. Immunization of BALB/c mice with the PADRE-Aβ1–15 epitope vaccine produced high titers of anti-Aβ Abs. Splenocytes from immunized mice showed robust T cell stimulation in response to peptides containing PADRE. However, splenocytes from immunized mice were not reactivated by the Aβ peptide. New preClinical Trials in amyloid precursor protein transgenic mouse models may help to develop novel immunogen-adjuvant configurations with the potential to avoid the adverse events that occurred in the first Clinical Trial.

Irina Petrushina - One of the best experts on this subject based on the ideXlab platform.

  • Prototype Alzheimer’s Disease Vaccine Using the
    2015
    Co-Authors: Promiscuous T Cell, Michael G. Agadjanyan, Anahit Ghochikyan, Irina Petrushina, Vitaly Vasilevko, Nina Movsesyan, Mikayel Mkrtichyan, Epitope Pan, Hla Dr-binding Peptide, Tommy Saing
    Abstract:

    Immunization of amyloid precursor protein transgenic mice with fibrillar -amyloid (A) prevents Alzheimer’s disease (AD)-like neuropathology. The first Immunotherapy Clinical Trial used fibrillar A, containing the B and T cell self epitopes of A, as the immunogen formulated with QS21 as the adjuvant in the vaccine. Unfortunately, the Clinical Trial was halted during the phase II stage when 6 % of the participants developed meningoencephalitis. The cause of the meningoencephalitis in the patients that received the vaccine has not been definitively determined; however, analysis of two case reports from the AN-1792 vaccine Trial suggest that the meningoencephalitis may have been caused by a T cell-mediated autoimmune response, whereas production of anti-A Abs may have been therapeutic to the AD patients. Therefore, to reduce the risk of an adverse T cell-mediated immune response to A Immunotherapy we have designed a prototype epitope vaccine that contains the immunodominant B cell epitope of A in tandem with the synthetic universal Th cell pan HLA DR epitope, pan HLA DR-binding peptide (PADRE). Importantly, the PADRE-A1–15 sequence lacks the T cell epitope of A. Immunization of BALB/c mice with the PADRE-A1–15 epitope vaccine produced high titers of anti-A Abs. Splenocytes from immunized mice showed robust T cell stimulation in response to peptides containing PADRE. However, splenocytes from immunized mice were not reactivated by the A peptide. New preClinical Trials in amyloid precursor protein transgenic mouse models may help to develop novel immunogen-adjuvant configurations with the potential to avoid the adverse events that occurred in the first Clinical Trial. The Journal of Immunology, 2005, 174: 1580–1586. A lzheimer’s disease (AD)4 is the most common form ofdementia in the elderly and is characterized by a pro-gressive loss of memory and a general cognitive decline

  • prototype alzheimer s disease vaccine using the immunodominant b cell epitope from β amyloid and promiscuous t cell epitope pan hla dr binding peptide
    Journal of Immunology, 2005
    Co-Authors: Michael G. Agadjanyan, Anahit Ghochikyan, Irina Petrushina, Vitaly Vasilevko, Nina Movsesyan, Mikayel Mkrtichyan, Tommy Saing, David H. Cribbs
    Abstract:

    Immunization of amyloid precursor protein transgenic mice with fibrillar β-amyloid (Aβ) prevents Alzheimer’s disease (AD)-like neuropathology. The first Immunotherapy Clinical Trial used fibrillar Aβ, containing the B and T cell self epitopes of Aβ, as the immunogen formulated with QS21 as the adjuvant in the vaccine. Unfortunately, the Clinical Trial was halted during the phase II stage when 6% of the participants developed meningoencephalitis. The cause of the meningoencephalitis in the patients that received the vaccine has not been definitively determined; however, analysis of two case reports from the AN-1792 vaccine Trial suggest that the meningoencephalitis may have been caused by a T cell-mediated autoimmune response, whereas production of anti-Aβ Abs may have been therapeutic to the AD patients. Therefore, to reduce the risk of an adverse T cell-mediated immune response to Aβ Immunotherapy we have designed a prototype epitope vaccine that contains the immunodominant B cell epitope of Aβ in tandem with the synthetic universal Th cell pan HLA DR epitope, pan HLA DR-binding peptide (PADRE). Importantly, the PADRE-Aβ1–15 sequence lacks the T cell epitope of Aβ. Immunization of BALB/c mice with the PADRE-Aβ1–15 epitope vaccine produced high titers of anti-Aβ Abs. Splenocytes from immunized mice showed robust T cell stimulation in response to peptides containing PADRE. However, splenocytes from immunized mice were not reactivated by the Aβ peptide. New preClinical Trials in amyloid precursor protein transgenic mouse models may help to develop novel immunogen-adjuvant configurations with the potential to avoid the adverse events that occurred in the first Clinical Trial.

  • prototype alzheimer s disease vaccine using the immunodominant b cell epitope from β amyloid and promiscuous t cell epitope pan hla dr binding peptide
    Journal of Immunology, 2005
    Co-Authors: Michael G. Agadjanyan, Anahit Ghochikyan, Irina Petrushina, Vitaly Vasilevko, Nina Movsesyan, Mikayel Mkrtichyan, Tommy Saing, David H. Cribbs
    Abstract:

    Immunization of amyloid precursor protein transgenic mice with fibrillar beta-amyloid (Abeta) prevents Alzheimer's disease (AD)-like neuropathology. The first Immunotherapy Clinical Trial used fibrillar Abeta, containing the B and T cell self epitopes of Abeta, as the immunogen formulated with QS21 as the adjuvant in the vaccine. Unfortunately, the Clinical Trial was halted during the phase II stage when 6% of the participants developed meningoencephalitis. The cause of the meningoencephalitis in the patients that received the vaccine has not been definitively determined; however, analysis of two case reports from the AN-1792 vaccine Trial suggest that the meningoencephalitis may have been caused by a T cell-mediated autoimmune response, whereas production of anti-Abeta Abs may have been therapeutic to the AD patients. Therefore, to reduce the risk of an adverse T cell-mediated immune response to Abeta Immunotherapy we have designed a prototype epitope vaccine that contains the immunodominant B cell epitope of Abeta in tandem with the synthetic universal Th cell pan HLA DR epitope, pan HLA DR-binding peptide (PADRE). Importantly, the PADRE-Abeta(1-15) sequence lacks the T cell epitope of Abeta. Immunization of BALB/c mice with the PADRE-Abeta(1-15) epitope vaccine produced high titers of anti-Abeta Abs. Splenocytes from immunized mice showed robust T cell stimulation in response to peptides containing PADRE. However, splenocytes from immunized mice were not reactivated by the Abeta peptide. New preClinical Trials in amyloid precursor protein transgenic mouse models may help to develop novel immunogen-adjuvant configurations with the potential to avoid the adverse events that occurred in the first Clinical Trial.

  • Prototype Alzheimer’s Disease Vaccine Using the Immunodominant B Cell Epitope from β-Amyloid and Promiscuous T Cell Epitope Pan HLA DR-Binding Peptide
    Journal of Immunology, 2005
    Co-Authors: Michael G. Agadjanyan, Anahit Ghochikyan, Irina Petrushina, Vitaly Vasilevko, Nina Movsesyan, Mikayel Mkrtichyan, Tommy Saing, David H. Cribbs
    Abstract:

    Immunization of amyloid precursor protein transgenic mice with fibrillar β-amyloid (Aβ) prevents Alzheimer’s disease (AD)-like neuropathology. The first Immunotherapy Clinical Trial used fibrillar Aβ, containing the B and T cell self epitopes of Aβ, as the immunogen formulated with QS21 as the adjuvant in the vaccine. Unfortunately, the Clinical Trial was halted during the phase II stage when 6% of the participants developed meningoencephalitis. The cause of the meningoencephalitis in the patients that received the vaccine has not been definitively determined; however, analysis of two case reports from the AN-1792 vaccine Trial suggest that the meningoencephalitis may have been caused by a T cell-mediated autoimmune response, whereas production of anti-Aβ Abs may have been therapeutic to the AD patients. Therefore, to reduce the risk of an adverse T cell-mediated immune response to Aβ Immunotherapy we have designed a prototype epitope vaccine that contains the immunodominant B cell epitope of Aβ in tandem with the synthetic universal Th cell pan HLA DR epitope, pan HLA DR-binding peptide (PADRE). Importantly, the PADRE-Aβ1–15 sequence lacks the T cell epitope of Aβ. Immunization of BALB/c mice with the PADRE-Aβ1–15 epitope vaccine produced high titers of anti-Aβ Abs. Splenocytes from immunized mice showed robust T cell stimulation in response to peptides containing PADRE. However, splenocytes from immunized mice were not reactivated by the Aβ peptide. New preClinical Trials in amyloid precursor protein transgenic mouse models may help to develop novel immunogen-adjuvant configurations with the potential to avoid the adverse events that occurred in the first Clinical Trial.

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