45 results about "Spongiform encephalopathy" patented technology

The invention provides cloned transgenic ungulates (e.g., bovines) in which prion protein activity is reduced by one or more genetically engineered mutations. Desirably, these transgenic bovines are also genetically modified to express xenogenous (e.g., human) antibodies. Because of their resistance to prion-related diseases such as bovine spongiform encephalopy (also known as mad cow disease), these bovines are a safer source of human antibodies for pharmaceutical uses and a safer source of agricultural products.

Assays are provided for rapid detection, with high specificity of the pathogenic form of prion protein responsible for neurodegenerative diseases affecting humans and animals, such as transmissible spongiform encephalopathy in bovine, sheep, and cats. Also provided are assays for testing animal feedstock, such as animal feed, for the presence or concentration of pathogenic prion protein. Results are available in from about 0.5 to about 20 minutes and preferably within from about 5 to about 10 minutes. The assays employ proteinase-K to remove normal prion protein from a biological sample, so that the sample may be analyzed by immunochromatography to determine the presence and concentration of pathogenic prion protein. Because the proteinase-K is immobilized on a solid support for in situ removal of interfering components, the present invention obviates the need for subsequent extraction of the desired analyte. All aspects of the present invention are suitable for quantifying the minimal detectable amount of pathogenic prion protein in a biological sample. Moreover, the simplicity of sample preparation makes the present invention suitable for use in the field.

Disclosed herein are compounds and methods for decreasing PrP and preventing, ameliorating, or treating a prion disease or conformational neurodegenerative disorder, in an individual in need thereof. Examples of disease conditions that can be ameliorated with the administration of antisense compounds targeted to PrP include Creutzfeldt-Jakob disease (CJD); variant Creutzfeldt-Jakob Disease (vCJD); Gerstmann-Straussler-Scheinker syndrome; fatal familial insomnia; kuru; Bovine Spongiform Encephalopathy (BSE), e.g. “mad cow disease”; Chronic Wasting Disease (CWD); scrapie; transmissible mink encephalopathy; feline spongiform encephalopathy; ungulate spongiform encephalopathy; Alzheimer's disease; Parkinson's disease; Huntington's disease; and Amyotrophic Lateral Sclerosis (ALS).

The present invention deals with a method of preparing nucleic acids, particularly RNA, from a whole blood sample. The nucleic acids purified by the method of the invention are particularly suited for detection of nucleic acid marker molecules. Preferred are markers for the diagnosis of transmissible spongiform encephalopathy (TSE). Such diagnosis is based on the detection, by means of real-time PCR, of certain mRNAs of the TSE-infected organism. Said mRNAs specifically originate as splicing variants and are isolated from whole blood by the method of the invention.

Embodiments of the present invention include methods and systems for designing inhibitors of amyloidosis in humans, domesticated animals, and wild animals as well as inhibitors of amyloidosis designed by the methods and systems. Methods and systems for designing inhibitors of amyloidosis are largely computational, in nature, and are directed to designing various types of polymers, small-molecule organic compounds, organometallic compounds, or non-chemical physical processes that can target the extended-α-strand and α-sheet regions of amyloidogenic protein and polypeptide intermediates in order to prevent aggregation of those intermediates into protofibrils and fibrils that, in turn, recruit additional native-conformation proteins and polypeptides into amyloidogenic intermediates and that additionally aggregate to form higher-order structures, such as plaques observed in the brains of patients suffering from the various spongiform encephalopathies.