Abstract: The present invention relates to a modified pig as a model for studying Alzheimer's disease. The modified pig model displays one or more phenotypes associated with Alzheimer's disease. Disclosed is also a modified pig comprising a modified human and/or porcine APP gene, and/or PS1 gene, and/or a transcriptional and/or translational product or part thereof. The invention further relates to methods for producing the modified pig; and methods for evaluating the effect of a therapeutical treatment of Alzheimer's disease; methods for screening the efficacy of a pharmaceutical composition; and a method for treatment of a human being suffering from Alzheimer's disease are disclosed.
Type:
Application
Filed:
March 6, 2008
Publication date:
June 3, 2010
Applicant:
AARHUS UNIVERSITET
Inventors:
Arne Lund Jorgensen, Ida Elisabeth Holm, Anders Lade Nielsen, Marianne Gregers Johansen, Jannik Ejnar Jakobsen
Abstract: A biomarker for Alzheimer's disease (AD) comprising a complex of an A? amyloid peptide and a cell or a cellular membrane. Non-invasive methods for diagnosing Alzheimer's disease or monitoring its development or progression using this biomarker.
Type:
Application
Filed:
April 30, 2013
Publication date:
October 31, 2013
Applicants:
Centre National de la Recherche Scientifique, Innovative Health Diagnostics
Inventors:
Corinne MBEBI-LIEGEOIS, Jean De Barry, Francois Sellal
Abstract: Disclosed are transgenic animals and transfected cell lines expressing a protein associated with Alzheimer's Disease, neuroectodermal tumors, malignant astrocytomas, and glioblastomas. Also disclosed is the use of such transgenic animals and transfected cell lines to screen potential drug candidates for treating or preventing Alzheimer's disease, neuroectodermal tumors, malignant astrocytomas, and glioblastomas. The invention also relates to new antisense oligonucleotides, ribozymes, triplex forming DNA and external guide sequences that can be used to treat or prevent Alzheimer's disease, neuroectodermal tumors, malignant astrocytomas, and glioblastomas.
Abstract: Disclosed are transgenic animals and transfected cell lines expressing a protein associated with Alzheimer's Disease, neuroectodermal tumors, malignant astrocytomas, and glioblastomas. Also disclosed is the use of such transgenic animals and transfected cell lines to screen potential drug candidates for treating or preventing Alzheimer's disease, neuroectodermal tumors, malignant astrocytomas, and glioblastomas. The invention also relates to new antisense oligonucleotides, ribozymes, triplex forming DNA and external guide sequences that can be used to treat or prevent Alzheimer's disease, neuroectodermal tumors, malignant astrocytomas, and glioblastomas.
Abstract: Disclosed are transgenic animals and transfected cell lines expressing a protein associated with Alzheimer's Disease, neuroectodermal tumors, malignant astrocytomas, and glioblastomas. Also disclosed is the use of such transgenic animals and transfected cell lines to screen potential drug candidates for treating or preventing Alzheimer's disease, neuroectodermal tumors, malignant astrocytomas, and glioblastomas. The invention also relates to new antisense oligonucleotides, ribozymes, triplex forming DNA and external guide sequences that can be used to treat or prevent Alzheimer's disease, neuroectodermal tumors, malignant astrocytomas, and glioblastomas.
Abstract: A method of generating a cellular model of Alzheimer's disease (AD) comprises integrating AD related gene to hiPSC to induce increased beta secretase and/or Abeta 42 peptides, and the cellular model of Alzheimer's disease (AD) is prepared by the method.
Abstract: A soluble derivative of low-density lipoprotein receptor related protein-1 (sLRP-1) binds directly to Alzheimer's amyloid-? peptide (A?). This binding may be used to detect A? or to separate A? from the rest of a subject's body. In Alzheimer's disease, it may be used to provide diagnostic results by detecting A?, treatment by removing A?, or both.
Type:
Application
Filed:
October 27, 2009
Publication date:
May 13, 2010
Applicants:
The University of Rochester, Socratech L.L.C.
Abstract: The present invention provides methods and compositions for screening, diagnosis and prognosis of Alzheimer's disease, for monitoring the effectiveness of Alzheimer's disease treatment, and for drug development. Alzheimer's Disease-Associated Features (AFs), detectable by two-dimensional electrophoresis of cerebrospinal fluid, serum or plasma are described. The invention further provides Alzheimer's Disease-Associated Protein Isoforms (APIs) detectable in cerebrospinal fluid, serum or plasma, preparations comprising isolated APIs, antibodies, pharmaceutical compositions, diagnostic and therapeutic methods, and kits comprising or based on the same.
Type:
Application
Filed:
April 3, 2001
Publication date:
November 7, 2002
Inventors:
L. Kathryn Durham, David L. Friedman, Herath Mudiyanselage Athula Chandrasiri Herath, Lida H. Kimmel, Rajesh Bhikhu Parekh, David M. Potter, Christian Rohlff, B. Michael Silber, Thomas R. Stiger, P. Trey Sunderland, Robert Reid Townsend, W. Frost White, Stephen A. Williams
Abstract: Model systems of Alzheimer's disease comprise a DNA sequence encoding an amyloid precursor protein (APP) isoform or fragment that has an amino acid substitution. The substituted amino acid may be other than valine at the amino acid position corresponding to amino acid residue position 717 of APP770. Methods of determining genetic predisposition to Alzheimer's disease are also disclosed.
Type:
Application
Filed:
February 3, 2003
Publication date:
September 4, 2003
Applicant:
Elan Pharmaceuticals
Inventors:
John Anthony Hardy, Marie-Christine Chartier-Harlin, Alison Mary Goate, Michael John Owen, Michael John Mullan
Abstract: The present invention relates to immunogenic compositions and peptides comprising residues 4-10 (FRHDSGY) of the amyloid peptide Abeta42. The invention further relates to antibodies that bind to the Abeta(4-10) antigenic determinant. The invention provides methods for treating Alzheimer's disease and for reducing the amyloid load in Alzheimers patients. The invention also relates to methods for designing small molecule inhibitors of amyloid deposition.
Type:
Application
Filed:
April 10, 2003
Publication date:
December 18, 2003
Applicant:
Hospital for Sick Children and University of Toronto
Inventors:
Peter H. St. George-Hyslop, JoAnne McLaurin
Abstract: The present invention provides materials and methods for treating Alzheimer's disease and other tau related neurodegenerative disorders. A tau kinase, Brain Derived Tau Kinase (BDTK) is provided. BDTK can cause hyperphosphorylation of tau protein, which leads to formation of neurofibrillary tangles, which are implicated in the degenerative symptoms of Alzheimer's and other neurodegenerative disorders. Methods of diagnosis and treatment based on the discovery of this novel tau kinase are also provided.
Abstract: Transgenic cell and animal models for Alzheimer's disease are described. Cells of the animals and the cell models themselves comprise a recombinant DNA construct comprising a control sequence and, under the control of the control sequence, a DNA sequence encoding a kinase that is capable, directly or indirectly, of modulating the phosphorylation of the microtubule-forming protein tau. The transgenic cells and animals may be used for testing potential therapeutic agents for Alzheimer's disease.
Type:
Grant
Filed:
August 23, 1996
Date of Patent:
November 30, 1999
Assignee:
King's College London
Inventors:
Brian H. Anderton, Christopher C. Miller
Abstract: Model systems of Alzheimer's disease comprise a DNA sequence encoding an amyloid precursor protein (APP) isoform or fragment that has an amino acid substitution. The substituted amino acid may be other than valine at the amino acid position corresponding to amino acid residue position 717 of APP770. Methods of determining genetic predisposition to Alzheimer's disease are also disclosed.
Type:
Grant
Filed:
January 21, 1992
Date of Patent:
March 2, 1999
Assignee:
Imperial College of Science, Technology of Medicine
Inventors:
John Anthony Hardy, Marie-Christine Chartier-Harlin, Alison Mary Goate, Michael John Owen, Michael John Mullan
Abstract: Nucleic acid molecules, including antisense and enzymatic nucleic acid molecules, such as hammerhead ribozymes, DNAzymes, and antisense, which modulate the expression of molecular targets impacting the development and progression of Alzheimer's disease, in particular, the expression of BACE and ps-2 gene.
Abstract: A method of screening pharmaceutical drugs, gene therapies, vaccines, dietary supplements, behavioral and environmental therapies and other clinical treatments for potential efficacy in the treatment of Alzheimer's disease in humans. The method includes selecting transgenic mice that are genetically altered for Alzheimer's disease and using measurement and/or imaging techniques to determine the activity level of the posterior cingulate region of the brains of the mice after treatment. Based on these measurements and comparisons to a control group, the effectiveness of the treatment in arresting or reversing Alzheimer's disease in mice can be determined, and the treatment can be identified as a promising candidate for human trials.
Abstract: Disclosed are transgenic animals and transfected cell lines expressing a protein associated with Alzheimer's Disease, neuroectodermal tumors, malignant astrocytomas, and glioblastomas. Also disclosed is the use of such transgenic animals and transfected cell lines to screen potential drug candidates for treating or preventing Alzheimer's disease, neuroectodermal tumors, malignant astrocytomas, and glioblastomas. The invention also relates to new antisense oligonucleotides, ribozymes, triplex forming DNA and external guide sequences that can be used to treat or prevent Alzheimer's disease, neuroectodermal tumors, malignant astrocytomas, and glioblastomas.
Abstract: The present invention relates to modified brain slice cultures and assay systems based thereon. In particular, the invention relates to a tissue-based assay system for screening agents capable of modulating etiopathology of neuronal cells, in particular in the context of Alzheimer's disease related brain lesions.
Abstract: The disclosure relates generally to neurodegenerative disorders and more specifically to a group of presenilin/G-protein/c-src binding polypeptides and methods of use for modulating signaling and progression of Alzheimer's disease.
Type:
Application
Filed:
May 12, 2009
Publication date:
December 10, 2009
Applicant:
THE REGENTS OF THE UNIVERSITY OF CALIFORNIA
Abstract: Tryptamine, a normal constituent of the diet and an inhibitor of tryptophanyl-tRNA synthetase (TrpRS), induces formation of Alzheimer's disease characteristics as extracellular senile plaques and neurofibrillary tangles containing paired helical neurofilaments and/or straight neurofilaments in human differentiated neuronal cells. The effect of tryptamine on neuronal cells is dose-dependent and multi-staged resulting in differentiation and subsequently axon growth, followed by neurodegeneration. TrpRS was found normally in the neuronal body, axons and dendrites, whereas tryptamine induces it in the cytoskeleton. In tryptamine-treated cells, TrpRS co-localized with abnormally phosphorylated tau in neurofibrillary tangles and with &bgr;-amyloid in senile plaque-like formations. Moreover, TrpRS was detected in neurofibrillary tangles and congophilic senile plaques in Alzheimer's disease brain sections and brain sections of model mice following tryptamine treatment.