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1. 发明专利

AU721869B2 Treatment of alzheimer disease by modulation of synapsins 未知
公开(公告)号：AU721869B2
公开(公告)日：2000-07-13
申请号：AU5745696
申请日：1996-05-13
申请人： UNIV ROCKEFELLER , BRIGHAM & WOMENS HOSPITAL
发明人： HAN HUI-QUAN , GREENGARD PAUL , KOSIK KENNETH S , FERREIRA ADRIANA
IPC分类号： A61K45/00 , A61K31/465 , A61K31/565 , A61K31/7052 , A61K38/00 , A61K38/18 , A61K38/22 , A61P25/00 , A61P25/28 , A61K31/70
摘要： The role of synapsin II in both the reformation and the maintenance of synaptic connections in cultured hippocampal neurons can be the basis of therapy for neurodegenerative disorder, particularly Alzheimer disease, which involve the disruption of synapses. When synapsin II expression in neurons is blocked by antisense synapsin II oligonucleotides, the ability of hippocampal neurons to reform as well as to maintain synapses is severely disrupted. Antisense suppression of synapsin II after axon formation but immediately before synaptogenesis prevents synapse formation. Suppression of synapsin II after synaptogenesis disrupts the majority of existing synapses. Re-expression of synapsin II in synapsin deficient neurons achieved after removing the antisense oligonucleotides leads to the re-establishment of synaptic connections, providing direct evidence that synapsin II is required for the maintenance and/or restoration of synapses. Thus, therapeutic methods based on the reformation and the maintenance of synapses, including delivery of the synapsin cDNAS or proteins into the patient's nervous system, use of the synapsin cDNAS to promote the synapse forming ability of cells for grafting, and use of agents that increase the expression of, enhancing the activity of, or mimic the activity of, the endogenous synapsins, can provide treatment of neurodegenerative disorders.

2. 发明专利

AU5745696A Treatment of alzheimer disease by modulation of synapsins 未知
公开(公告)号：AU5745696A
公开(公告)日：1996-11-29
申请号：AU5745696
申请日：1996-05-13
申请人： UNIV ROCKEFELLER , BRIGHAM & WOMENS HOSPITAL
发明人： HAN HUI-QUAN , GREENGARD PAUL , KOSIK KENNETH S , FERREIRA ADRIANA
IPC分类号： A61K45/00 , A61K31/465 , A61K31/565 , A61K31/7052 , A61K38/00 , A61K38/18 , A61K38/22 , A61P25/00 , A61P25/28 , A61K31/70
摘要： The role of synapsin II in both the reformation and the maintenance of synaptic connections in cultured hippocampal neurons can be the basis of therapy for neurodegenerative disorder, particularly Alzheimer disease, which involve the disruption of synapses. When synapsin II expression in neurons is blocked by antisense synapsin II oligonucleotides, the ability of hippocampal neurons to reform as well as to maintain synapses is severely disrupted. Antisense suppression of synapsin II after axon formation but immediately before synaptogenesis prevents synapse formation. Suppression of synapsin II after synaptogenesis disrupts the majority of existing synapses. Re-expression of synapsin II in synapsin deficient neurons achieved after removing the antisense oligonucleotides leads to the re-establishment of synaptic connections, providing direct evidence that synapsin II is required for the maintenance and/or restoration of synapses. Thus, therapeutic methods based on the reformation and the maintenance of synapses, including delivery of the synapsin cDNAS or proteins into the patient's nervous system, use of the synapsin cDNAS to promote the synapse forming ability of cells for grafting, and use of agents that increase the expression of, enhancing the activity of, or mimic the activity of, the endogenous synapsins, can provide treatment of neurodegenerative disorders.

3. 发明专利

CA2220897A1 TREATMENT OF ALZHEIMER DISEASE BY MODULATION OF SYNAPSINS 未知
公开(公告)号：CA2220897A1
公开(公告)日：1996-11-14
申请号：CA2220897
申请日：1996-05-13
申请人： UNIV ROCKEFELLER , BRIGHAM & WOMENS HOSPITAL
发明人： GREENGARD PAUL , KOSIK KENNETH S , FERREIRA ADRIANA , HAN HUI-QUAN
IPC分类号： A61K45/00 , A61K31/465 , A61K31/565 , A61K31/7052 , A61K38/00 , A61K38/18 , A61K38/22 , A61P25/00 , A61P25/28 , A61K38/17 , A61K38/19 , A61K31/70
摘要： The role of synapsin II in both the reformation and the maintenance of synaptic connections in cultured hippocampal neurons can be the basis of therapy for neurodegenerative disorder, particularly Alzheimer disease, which involve the disruption of synapses. When synapsin II expression in neurons is blocked by antisense synapsin II oligonucleotides, the ability of hippocampal neurons to reform as well as to maintain synapses is severely disrupted. Antisense suppression of synapsin II after axon formation but immediately before synaptogenesis prevents synapse formation. Suppression of synapsin II after synaptogenesis disrupts the majority of existing synapses. Re-expression of synapsin II in synapsin deficient neurons achieved after removing the antisense oligonucleotides leads to the re-establishment of synaptic connections, providing direct evidence that synapsin II is required for the maintenance and/or restoration of synapses. Thus, therapeutic methods based on the reformation and the maintenance of synapses, including delivery of the synapsin cDNAS or proteins into the patient's nervous system, use of the synapsin cDNAS to promote the synapse forming ability of cells for grafting, and use of agents that increase the expression of, enhancing the activity of, or mimic the activity of, the endogenous synapsins, can provide treatment of neurodegenerative disorders.

4. 发明专利

MX9708736A TRATAMIENTO DE LA ENFERMEDAD DE ALZHEIMER MEDIANTE LA MODULACION DE SINAPSINAS. 未知
公开(公告)号：MX9708736A
公开(公告)日：1998-06-28
申请号：MX9708736
申请日：1997-11-12
申请人： ROCKEFELLER UNVERSITY , BRIGHAM & WOMENS HOSPITAL
发明人： HAN HUI-QUAN , GREENGARD PAUL , KOSIK KENNETH S , FERREIRA ADRIANA
IPC分类号： A61K45/00 , A61K31/465 , A61K31/565 , A61K31/7052 , A61K38/00 , A61K38/18 , A61K38/22 , A61P25/00 , A61P25/28 , A61K31/70
摘要： La funcion de la sinapsina II tanto en la reformacion como en el mantenimiento de las conexiones sinápticas en neuronas de hipocampo cultivadas, puede se la base de la terapia para trastornos neurodegenerativos, particularmente la enfermedad de Alzheimer, que implica la interrupcion de las sinapsis; cuando la expresion de la sinapsina II en neuronas es bloqueada por los oligonucleotidos de antisentido para sinapsina II, la capacidad de las neuronas de hipocampo para volver a formar, así como para mantener la sinapsis, se interrumpe severamente; la supresion de antisentido de la sinapsina II después de la formacion del axon, pero inmediatamente antes de la sinaptogénesis, impide la formacion de la sinapsis, la supresion de la sinapsina II después de la sinaptogénesis interrumpe la mayoría de las sinapsis existentes; la reexpresion de la sinapsina II en neuronas deficientes en sinapsina, lograda después de remover los oligonucleotidos de antisentido, da como resultado el reestablecimiento de conexiones sinápticas, dando evidencia directa de que la sinapsina II se requiere para el mantenimiento y/o la restauracion de las sinapsis; así, los métodos terapéuticos basados en la reformacion y el mantenimiento de las sinapsis, incluyendo la liberacion de las moléculas de ADNc o proteínas de sinapsina en el sistema nervioso del paciente, el uso de moléculas de ADNc de sinapsina para promover la capacidad de las células para formar sinapsis para injerto, y el uso de agentes que incrementan la expresion de las sinapsinas endogenas -- incrementando o simulando la actividad de las mismas --, pueden proveer tratamiento de trastornos neurodegenerativos.

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