-
公开(公告)号：EP1532258A1
公开(公告)日：2005-05-25
申请号：EP03757480.3
申请日：2003-06-11
CPC分类号： G01N33/6896 , G01N2800/2821 , G01N2800/52
摘要： Dysregulation of vascular function is observed in brain endothelium derived from patients affected by Alzheimer's disease. This may be manifested at the cell or organ level: e.g., abnormal capillary morphogenesis, defective angiogenesis, inappropriate cellular senescence, mitotic catastrophe, or combinations thereof. This observation can be used for diagnosis or treatment of neurodegenerative disorders and other cognitive impairments.
-
2.发明公开SERUM RESPONSE FACTOR AND MYOCARDIN CONTROL ALZHEIMER CEREBRAL AMYLOID ANGIOPATHY 审中-公开血清反应因子和MYOKARDIN控制阿尔茨海默氏HRIN淀粉样血管病
公开(公告)号：EP1948198A2
公开(公告)日：2008-07-30
申请号：EP06844353.0
申请日：2006-11-14
CPC分类号： A61K48/00 , C12N15/113 , C12N2310/14 , C12N2310/531
摘要： Cerebral amyloid angiopathy is involved in Alzheimer dementia through reduction in arterial blood flow that may impair protein synthesis, which is required for learning and memory, and lower the threshold for ischemic injury. Elevated serum response factor (SRF) or myocardin (MYOCD) activity in subjects afflicted by or at risk for development of Alzheimer's disease (AD) promotes a 'vascular smooth muscle cell' (VSMC) hypercontractile phenotype in brain arteries and enhance accumulation of Aβ in the vessel wall. This, in turn, can initiate a disease process in cerebral arteries which can cause brain arterial hypoperfusion and neurovascular uncoupling, that are commonly seen in AD. Thus, SRF and MYOCD represent novel targets for treating arterial dysfunction associated with cognitive decline in AD.
-
公开(公告)号：EP1572134A2
公开(公告)日：2005-09-14
申请号：EP03799306.0
申请日：2003-09-30
IPC分类号： A61K7/00
CPC分类号： C07K14/8128 , A61K38/36 , G01N2500/10 , G01N2510/00
摘要： Protein S is a significant neuroprotectant when administered after focal ischemic stroke and prevents hypoxic/re-oxygenation injury. Purified human plasma-derived or recombinant protein S improves motor neurological function after stroke, and reduced brain infarction and edema. Protein S also enhances post-ischemic reperfusion and reduced brain fibrin and neutrophil deposition. Cortical neurons are protected from hypoxia/re-oxygenation-induced apoptosis. Thus, protein S and variants thereof are prototypes of a class of agents for preventing injury of the nervous system. In particular, a disease or other pathological condition (e.g., stroke) may be treated with such agents having one or more protein S activities (e.g., anti-thrombotic and anti-inflammatory activities, direct cellular neuronal protective effects) although the latter activities are not be required.
-
4.发明公开INHIBITING AMYLOID-BETA PEPTIDE/RAGE INTERACTION AT THE BLOOD-BRAIN BARRIER 审中-公开抑制淀粉样-β-肽/ RAGE相互作用。在血液 - 脑屏障
公开(公告)号：EP1993527A2
公开(公告)日：2008-11-26
申请号：EP07762687.7
申请日：2007-01-26
IPC分类号： A61K31/16
CPC分类号： A61K31/166 , A61K31/167
摘要： Small molecules are used to inhibit specific receptor-ligand interaction between Alzheimer's amyloid-β peptide (Aβ) and Receptor for Advanced GIy- cation Endproducts (RAGE). Objectives include treating Alzheimer's disease and other pathologies involving cerebral amyloid angiopathy; improving blood flow to or within the brain; decreasing the level of Aβ in the brain; reducing neuropathology associated with Alzheimer's disease; reducing inflammation and/or oxidant stress in the brain; improving memory and/or learning; treating other conditions involving Aβ/RAGE interaction at the blood-brain barrier, RAGE-mediated transport of Aβ into the brain, or RAGE activation in brain vasculature and/or brain parenchyma (e.g., diabetic complications); or any combination thereof.
-
公开(公告)号：EP1909574A2
公开(公告)日：2008-04-16
申请号：EP06800671.7
申请日：2006-08-03
CPC分类号： A61K48/005 , A61K48/0075
摘要： Neurovascular disorder critically contributes to the development and pathogenesis of Alzheimer's disease (AD). Transcriptional profiling of human brain endothelial cells (BEC) defines a subset of age-independent genes significantly altered in AD including the homebox gene GAX whose expression controls vascular phenotype and is low in AD. By using viral-mediated GAX gene silencing and transfer, restoring GAX expression in AD BEC is angiogenic, transcriptionally suppresses the AFX1 forkhead transcription factor- mediated apoptosis, and increases the levels of a major amyloid β-peptide (Aβ) clearance receptor, the low density lipoprotein receptor-related protein 1 (LRP- 1) at the blood-brain barrier. In a mouse model of Alzheimer's disease, deletion of the Gax gene results in reductions in brain capillary density and the resting cerebral blood flow, loss of angiogenic brain response to hypoxia, and an impaired Aβ brain efflux caused by reduced LRP-1 levels. The link of GAX gene to AD neurovascular dysfunction provides new mechanistic and therapeutic insights into AD.
-
6.发明公开ACTIVATED PROTEIN C INHIBITS UNDESIRABLE EFFECTS OF PLASMINOGEN ACTIVATOR IN THE BRAIN 审中-公开活化的蛋白C酶原抑制大脑中的不良反应
公开(公告)号：EP1773371A2
公开(公告)日：2007-04-18
申请号：EP05802434.0
申请日：2005-07-25
发明人： ZLOKOVIC, Berislav, V. , LIU, Dong , CHENG, Tong , GUO, Huang
CPC分类号： A61K38/4866 , A61K38/49 , A61K2300/00
摘要： Activated protein C (APC), a prodrug, and/or a variant of APC may be used to inhibit undesirable effects of plasminogen activator: e.g., apoptosis or cell death of neurons and endothelial cells, brain hemorrhage or intracerebral bleeding, and/or tissue damage in a subject’s brain. Inhibition appears to act through the extrinsic pathway of death receptor signal transduction. This represents an improvement in treatment using plasminogen activator (e.g., fibrinolysis). By reducing undesirable effects, the window for fibrinolythic therapy by plasminogen activator may be widened.
-
7.发明授权NEUROPROTECTIVE ACTIVITY OF ACTIVATED PROTEIN C IS INDEPENDENT OF ITS ANTICOAGULANT ACTIVITY 有权活化C蛋白的神经保护作用是独立的其抗凝血作用
公开(公告)号：EP1567199B1
公开(公告)日：2014-07-23
申请号：EP03790377.0
申请日：2003-12-05
CPC分类号： C12Y304/21069 , A61K38/08 , A61K38/4866 , G01N2333/4748 , G01N2333/96461 , G01N2510/00
-
公开(公告)号：EP1572134B1
公开(公告)日：2011-09-28
申请号：EP03799306.0
申请日：2003-09-30
CPC分类号： C07K14/8128 , A61K38/36 , G01N2500/10 , G01N2510/00
摘要： Protein S is a significant neuroprotectant when administered after focal ischemic stroke and prevents hypoxic/re-oxygenation injury. Purified human plasma-derived or recombinant protein S improves motor neurological function after stroke, and reduced brain infarction and edema. Protein S also enhances post-ischemic reperfusion and reduced brain fibrin and neutrophil deposition. Cortical neurons are protected from hypoxia/re-oxygenation-induced apoptosis. Thus, protein S and variants thereof are prototypes of a class of agents for preventing injury of the nervous system. In particular, a disease or other pathological condition (e.g., stroke) may be treated with such agents having one or more protein S activities (e.g., anti-thrombotic and anti-inflammatory activities, direct cellular neuronal protective effects) although the latter activities are not be required.
-
-
-
-
-
-
-
搜索结果
8 条记录 (耗时 0.016 秒)
