ES2325350T1 - Diagnostico de la enfermedad de alzheimer basado en una fosforilacion de proteina quinasa activada por agentes mitogenos. - Google Patents

Diagnostico de la enfermedad de alzheimer basado en una fosforilacion de proteina quinasa activada por agentes mitogenos. Download PDF

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ES2325350T1
ES2325350T1 ES08002964T ES08002964T ES2325350T1 ES 2325350 T1 ES2325350 T1 ES 2325350T1 ES 08002964 T ES08002964 T ES 08002964T ES 08002964 T ES08002964 T ES 08002964T ES 2325350 T1 ES2325350 T1 ES 2325350T1
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cells
alzheimer
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phosphorylation
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Wei-Qin Zhao
Daniel L. Alkon
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Blanchette Rockefeller Neuroscience Institute
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    • A61K31/5375—1,4-Oxazines, e.g. morpholine
    • A61K31/5377—1,4-Oxazines, e.g. morpholine not condensed and containing further heterocyclic rings, e.g. timolol
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    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
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    • A61P25/28—Drugs for disorders of the nervous system for treating neurodegenerative disorders of the central nervous system, e.g. nootropic agents, cognition enhancers, drugs for treating Alzheimer's disease or other forms of dementia
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    • G01N2800/28—Neurological disorders
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Abstract

Método de diagnóstico de la enfermedad de Alzheimer que comprende: poner en contacto células in vitro de un individuo con un agente que provoca la liberación de calcio intracelular a través del receptor del inositol 1,4,5-trifosfato (IP3), medir la cantidad de fosforilación de una proteína MAPK en las células del individuo in vitro en uno o más tiempos después de la etapa de contacto, y comparar la cantidad de fosforilación de la proteína MAPK en las células del individuo in vitro en uno o más tiempos con la cantidad de fosforilación en células de un individuo de control sin Alzheimer in vitro en los mismos tiempos después de poner en contacto las células de control con el agente, en el que la fosforilación aumentada de la proteína MAPK en las células del individuo comparada con las células de control, es un diagnóstico para la enfermedad de Alzheimer.

Claims (11)

1. Método de diagnóstico de la enfermedad de Alzheimer que comprende:
\quad
poner en contacto células in vitro de un individuo con un agente que provoca la liberación de calcio intracelular a través del receptor del inositol 1,4,5-trifosfato (IP3),
\quad
medir la cantidad de fosforilación de una proteína MAPK en las células del individuo in vitro en uno o más tiempos después de la etapa de contacto, y
\quad
comparar la cantidad de fosforilación de la proteína MAPK en las células del individuo in vitro en uno o más tiempos con la cantidad de fosforilación en células de un individuo de control sin Alzheimer in vitro en los mismos tiempos después de poner en contacto las células de control con el agente,
\quad
en el que la fosforilación aumentada de la proteína MAPK en las células del individuo comparada con las células de control, es un diagnóstico para la enfermedad de Alzheimer.
2. Método, según la reivindicación 1, en el que el agente es bradiquinina, un agonista del receptor de la bradiquinina o bombesina.
3. Método, según la reivindicación 1 ó 2, en el que la proteína MAPK es Erk1/2.
4. Método, según cualquiera de las reivindicaciones 1 a 3, en el que las células son fibroblastos de piel.
5. Método para el cribado de compuestos para la identificación de un compuesto útil para el tratamiento o prevención de la enfermedad de Alzheimer, que comprende:
\quad
poner en contacto células de prueba de un individuo con AD con un compuesto que se está cribando,
\quad
estimular las células de prueba antes, durante o después de la etapa de contacto con un agente que provoca la liberación del calcio intracelular a través del receptor del inositol 1,4,5-trifosfato (IP3),
\quad
medir la cantidad de fosforilación de la proteína MAPK en las células de prueba en uno o más tiempos después de la estimulación de las células de prueba,
\quad
comparar la cantidad de fosforilación de la proteína MAPK en las células de prueba en uno o más tiempos con la cantidad de fosforilación en el mismo tiempo o tiempos en las células de control de un individuo con AD que no se han puesto en contacto con el compuesto, y
\quad
aceptar un compuesto que inhibe o evita la fosforilación aumentada como compuesto principal, y rechazar un compuesto que no inhibe o evita la fosforilación aumentada.
6. Método, según la reivindicación 5, en el que el agente es bradiquinina o un agonista del receptor de bradiquinina.
7. Método, según la reivindicación 5 ó 6, en el que la proteína MAPK es Erk1/2.
8. Equipo de prueba de diagnóstico de la enfermedad de Alzheimer que comprende un anticuerpo anti-fosfo-proteína MAPK y bradiquinina.
9. Método de diagnóstico de la enfermedad de Alzheimer que comprende:
a) poner en contacto células de fibroblastos de piel in vitro de un individuo con una concentración de bradiquinina eficaz, estimuladora de la fosforilación;
b) poner en contacto células de fibroblastos de piel in vitro de un individuo de control sin Alzheimer con una concentración de bradiquinina eficaz, estimuladora de la fosforilación;
c) Medir la cantidad de Erk1/2 fosforilada en las células del individuo in vitro en uno o más tiempos seleccionados del grupo que consiste en 2 minutos, 5 minutos, 10 minutos, 20 minutos, y 30 minutos; mediante transferencia Western, utilizando un anticuerpo específico de fosfo Erk1/2;
d) Medir la cantidad de Erk1/2 fosforilada en las células in vitro de un individuo de control sin Alzheimer en el mismo tiempo o tiempos que en (c);
e) Normalizar la cantidad de Erk1/2 fosforilada en las etapas (c) y (d) a la cantidad de proteína presente en dichas células;
comparando la cantidad de Erk1/2 fosforilada en las células del individuo con la cantidad de Erk1/2 fosforilada en las células de control sin Alzheimer, en el que una cantidad aumentada de Erk1/2 fosforilada en las células del individuo comparada con la de las células de control sin Alzheimer es un diagnóstico para la enfermedad de
Alzheimer.
10. Método de cribado para la identificación de un compuesto útil para el tratamiento o la prevención de la enfermedad de Alzheimer que comprende:
a) poner en contacto fibroblastos de piel de prueba de un individuo con enfermedad de Alzheimer con un compuesto que se va a cribar;
b) poner en contacto fibroblastos de piel de control de dicho individuo con un agente de control para dicho compuesto o incubar dichos fibroblastos de piel de control en ausencia de dicho compuesto o bien de dicho agente de control;
c) estimular los fibroblastos de prueba y de control antes, durante o después del contacto en las etapas (a) y (b) con una concentración de bradiquinina eficaz, estimuladora de fosforilación;
d) medir la cantidad de Erk1/2 fosforilada en los fibroblastos de prueba y de control en uno o más tiempos seleccionados del grupo que consiste en 2 minutos, 5 minutos, 10 minutos, 20 minutos, y 30 minutos, mediante transferencia Western, utilizando un anticuerpo específico de fosfo Erk1/2, en el que la cantidad de Erk1/2 fosforilada se normaliza a la cantidad de proteína presente en dichos fibroblastos de prueba y de control;
e) comparar la cantidad de Erk1/2 fosforilada en los fibroblastos de prueba con la cantidad de Erk1/2 fosforilada en los fibroblastos de control para determinar si el compuesto inhibe o evita el aumento en fosforilación de Erk1/2 inducido por bradiquinina en las células de prueba comparado con las células de control, en el que un compuesto que inhibe o evita la fosforilación aumentada se identifica como útil para el tratamiento o prevención de la enfermedad de Alzheimer.
11. Utilización de un inhibidor de la fosforilación de MAPK, para la preparación de una composición farmacéutica para la reducción de la proteolisis de la proteína precursora de amiloide, la secreción de la proteína \beta amiloide, y/o la fosforilación de la proteína tau para tratar, de este modo, la enfermedad de Alzheimer, y el inhibidor de la fosforilación se selecciona del grupo que comprende: un inhibidor de la actividad de la proteína quinasa C, un inhibidor de la actividad de la proteína C-scr tirosina quinasa y un inhibidor del receptor de IP-3, en la que el inhibidor de la actividad de la proteína quinasa C es BiSM-1, el inhibidor de la actividad de la proteína C-scr tirosina quinasa es PP1 y el inhibidor del receptor de IP-3 es borato de 2-aminoetoxidifenilo.
ES08002964T 2001-02-27 2002-02-27 Diagnostico de la enfermedad de alzheimer basado en una fosforilacion de proteina quinasa activada por agentes mitogenos. Pending ES2325350T1 (es)

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US27141601P 2001-02-27 2001-02-27
US271416P 2001-02-27
US32950501P 2001-10-17 2001-10-17
US329505P 2001-10-17

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ES08002964T Pending ES2325350T1 (es) 2001-02-27 2002-02-27 Diagnostico de la enfermedad de alzheimer basado en una fosforilacion de proteina quinasa activada por agentes mitogenos.
ES02723236T Expired - Lifetime ES2305234T3 (es) 2001-02-27 2002-02-27 Diagnostico de la enfermedad de alzheimer basado en la fosforilacion de una proteina quinosa activada por mitogeno.

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US (3) US7682807B2 (es)
EP (1) EP1385531B1 (es)
JP (3) JP4246495B2 (es)
KR (2) KR100960256B1 (es)
CN (1) CN1549721B (es)
AT (1) ATE394115T1 (es)
AU (1) AU2002254029A1 (es)
DE (2) DE60226429D1 (es)
ES (2) ES2325350T1 (es)
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