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VACCINE FOR TREATMENT OF TAUTOPATHY UPDATE

外国特許コード F110005788
整理番号 2810
掲載日 2011年9月15日
出願国 世界知的所有権機関(WIPO)
国際出願番号 2011JP050616
国際公開番号 WO 2011083881
国際出願日 平成23年1月11日(2011.1.11)
国際公開日 平成23年7月14日(2011.7.14)
優先権データ
  • 特願2010-003424 (2010.1.8) JP
発明の名称 (英語) VACCINE FOR TREATMENT OF TAUTOPATHY UPDATE
発明の概要(英語) Disclosed is a vaccine for preventing or treating tautopathy, comprising a vector carrying a nucleic acid encoding a mutant tau protein linked to a secretion signal sequence as an active ingredient. The vaccine can induce an antibody against an (optionally phospholylated) tau protein in a subject in a further sustained manner compared with a case where the mutant tau protein is administered directly.
従来技術、競合技術の概要(英語) BACKGROUND ART
Tau in the normal brain protein is bound to the microtubules within the cell is present in the soluble phosphorylated protein, microtubule polymerization accelerators and stabilization of the contribute, deviates from the microtubule binding repeats are maintained in an equilibrium state. This equilibrium is phosphorylated, dephosphorylation enzyme is disrupted due to an error, free within the cytoplasm of the tau protein is increased, so as to appear to aggregation or fibrosis. Fronto-temporal dementia Alzheimer's disease including dementia of the elderly in the majority of, without necessarily amyloid accumulation, accumulation of tau protein aggregation in neurodegenerative disease can be recognized as characteristic for the lesion, are collectively referred to as ETLHI (non-patent document 1). 65 Years old or older Climate in dementia is observed at about 7%, about 10% reaches the mild dementia is applied. 7 Is the interrupt By ETLHI type dementia, the number of patients is about 200 million. Amyloid β dementia ongoing research and development up to now the prior research (A β) and protein, amyloid β peptide drug in a clinical immunity are performed, inoculated in the middle of the 6% patient clinical trial of the clinical trial which caused the meninges encephalitis are discontinued (non-patent document 2). Is taken out of the study, post-vaccinal encephalitis occurs after frequent interruptions, different disease for patients who died by case report, neurodegeneration senile plaques by vaccination was quenching effect of the projections has been confirmed (non-patent document 3). In addition, a subsequent follow-up vaccination studies, this vaccine administration, necropsy patients with confirmed the disappearance of the senile plaques also confirmed that the disease progresses, this vaccine is not effective in preventing the progression of the disease suggesting that the (non-patent document 4). In addition, the antibodies against amyloid β is effective in passive immunization studies showed that hitherto but, is known about the effect of suppressing the progress of the disease (non-patent document 5) is not. Adeno-associated virus (AAV) vector further equipped with an amyloid β verified the effect of the vaccine. In mice, this AAV vector through intestinal mucosa by oral administration of the antibody production against amyloid β effect, the effect of improving the learning function (non-patent document 6) was observed, then a decrease in the monkey experiments but was observed in senile plaques, a clear progression inhibitory effect was not ascertained. On the other hand, tau for proteins, such as far as a therapeutic target for treatment of Alzheimer's disease has not been great account, in recent years, an alternative to amyloid β protein with a therapeutic agent as a target for Alzheimer's, with excess accumulation of tau protein in the treatment and vaccine target ETLHI (non-patent document 7) becoming. As a therapeutic agent for connection with the present invention, adeno-associated virus gene encoding the amyloid β is mounted Alzheimer's therapeutic agent (Patent Document 1, 2, non-patent document 8), and by inoculation of the protein with a method of treating Alzheimer ETLHI (patent document 3, non-patent document 9) is reported and the like, or protein tau opal qi model mouse inoculated in coordinated movement, but the effect of improving learning motion was observed in the lack of social, a reduction in force congeneric dementia patients characteristically seen in the effect of improving symptoms have not been observed.
  • 出願人(英語)
  • ※2012年7月以前掲載分については米国以外のすべての指定国
  • KYOTO UNIVERSITY
  • NATIONAL INSTITUTE OF RADIOLOGICAL SCIENCES
  • 発明者(英語)
  • INOUE, Haruhisa
  • TAKEUCHI, Hiroki
  • TAKAHASHI, Ryosuke
  • HIGUCHI, Makoto
  • JI, Bin
  • SUHARA, Tetsuya
国際特許分類(IPC)
指定国 National States: AE AG AL AM AO AT AU AZ BA BB BG BH BR BW BY BZ CA CH CL CN CO CR CU CZ DE DK DM DO DZ EC EE EG ES FI GB GD GE GH GM GT HN HR HU ID IL IN IS JP KE KG KM KN KP KR KZ LA LC LK LR LS LT LU LY MA MD ME MG MK MN MW MX MY MZ NA NG NI NO NZ OM PE PG PH PL PT RO RS RU SC SD SE SG SK SL SM ST SV SY TH TJ TM TN TR TT TZ UA UG US UZ VC VN ZA ZM ZW
ARIPO: BW GH GM KE LR LS MW MZ NA SD SL SZ TZ UG ZM ZW
EAPO: AM AZ BY KG KZ MD RU TJ TM
EPO: AL AT BE BG CH CY CZ DE DK EE ES FI FR GB GR HR HU IE IS IT LT LU LV MC MK MT NL NO PL PT RO RS SE SI SK SM TR
OAPI: BF BJ CF CG CI CM GA GN GQ GW ML MR NE SN TD TG
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