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AGENT FOR AMELIORATING BLOOD-BRAIN BARRIER DISORDERS

外国特許コード F110005895
整理番号 S2009-0934-C0
掲載日 2011年11月9日
出願国 世界知的所有権機関(WIPO)
国際出願番号 2010JP063501
国際公開番号 WO 2011019023
国際出願日 平成22年8月9日(2010.8.9)
国際公開日 平成23年2月17日(2011.2.17)
優先権データ
  • 特願2009-185816 (2009.8.10) JP
発明の名称 (英語) AGENT FOR AMELIORATING BLOOD-BRAIN BARRIER DISORDERS
発明の概要(英語) A substance that can prevent the fragility of a blood-brain barrier which occurs upon the development of cerebral ischemia and can protect a blood-brain barrier has been keenly demanded. Disclosed is an agent for ameliorating blood-brain barrier disorders, which is characterized by comprising prothymosin-α or a protein or peptide having an equivalent function to that of prothymosin-α as an active ingredient. The agent can improve the fragility of a blood-brain barrier which may occur upon the development of cerebral ischemia and therefore can act as a therapeutic agent for diseases induced by blood-brain barrier disorders.
従来技術、競合技術の概要(英語) BACKGROUND ART
In the human brain is several hundred billion nerve cells of a complex network also is configured, from just a few of the neural stem cells if neural mechanism does not take into account, basically that number of cells, only decreases just after birth. Hundred and several tens years period referred to as a long service life, various exogenous, endogenous susceptible to stress caused by a variety of brain protection mechanism which is an advantage, and survival. With its own protection mechanisms of the brain glial or neuronal nerve - nerve - influence community present between the elevation role in order to maintain a working. The best known neuroprotective mechanism by the molecules such as cytokines and neurotrophic factors are in function. Under different stress conditions such neurotrophic factor is nerve cell death (apoptosis) to program to suppresses the known as having. The mechanisms of the nerve and another, in a recent report cerebral ischemia under stress when increased nerve has been reported that, because of the large amount of nerve cell death is not sufficient to compensate for expected.
Cerebral ischemia at the time of ischemia in the central portion of the core portion of the destructive cell death necrosis is observed, this cell death in order to dissipate the contents of the cells, the cytotoxic effects that would otherwise spread around the to-be-further. However several days after in the penumbra region referred to as the surrounding, condensation or fragmentation of cells, such as such as a phenomenon peculiar to the phagocytosis by microglia apoptosis is observed. Such apoptosis seen in the penumbra, localized to the injury site to prevent any injury throughout the brain by a type of protecting mechanism functions as considered (see non-patent document 1). The inventors, the above-described cerebral ischemia at the time of cell death from necrosis to apoptosis seen in the form of translation, which results in α is found for the first time (see non-patent document 2).
At 3 the mortality rate of the first Japanese stroke is however, important in the pathogenesis of bedridden at position 1 and the second disease, cerebral ischemia caused by the disease. Improve the outcome for stroke is acute treatment is important in the sense is called. The current method has been attracting attention as primary treatment for plasminogen activator (hereinafter, referred to as' tPA ') has been achieved is a thrombolytic agent, its use is limited within 3, the patient can receive the benefit from around ten (see non-patent document 3) only. This is with a lapse of time following a stroke and in order to weaken the blood-brain barrier, such as by the use of tPA thrombolytic agent increasing the risk of hemorrhagic stroke in some cases. However, such as thrombolytic agents can be used with, the blood-brain barrier from the blood-brain barrier to protect the weakening of a material having a function not yet to be discovered.
The inventors have recently, nerve cell death α material having a protective effect, this neuronal cell death by suppressive effects stroke reducing disturbances can be found for the first time the material (see Patent Document 1). The inventors of the present invention also relates to a mouse α , strokes and ischemia and glaucoma in rats has an effect of suppressing also found (see non-patent document 4-6).
  • 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
  • NAGASAKI UNIVERSITY
  • 発明者(英語)
  • UEDA, Hiroshi
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 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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