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Selection of Aptamers for Amyloid β-Protein, the Causative Agent of Alzheimer's Disease
Published on: May 13, 2010
La inducción exógena de la beta-amiloidogénesis cerebral está regida por el agente y el huésped
Melanie Meyer-Luehmann1, Janaky Coomaraswamy, Tristan Bolmont
1Department of Cellular Neurology, Hertie-Institute for Clinical Brain Research, University of Tübingen, D-72076 Tübingen, Germany.
Science (New York, N.Y.)
|September 23, 2006
Resumen
La agregación de proteínas de la enfermedad de Alzheimer se puede iniciar mediante la inyección de extractos cerebrales específicos. Estos extractos actúan como semillas, causando beta-amiloidosis y patología de una manera similar a las cepas priónicas.
Área de la Ciencia:
- La neurociencia es la neurociencia.
- Patología Patología Patología.
- La bioquímica es la bioquímica.
Sus antecedentes:
- La agregación de proteínas, en particular la beta-amiloide (Abeta), es un factor clave en la patogénesis de la enfermedad de Alzheimer (EA).
- Los mecanismos de iniciación in vivo de la agregación de Abeta siguen siendo en gran medida desconocidos.
Objetivo del estudio:
- Para investigar el inicio de la agregación de Abeta in vivo.
- Para determinar si el Abeta exógeno puede sembrar amiloidosis en un organismo vivo.
- Explorar las características de la amiloidosis inducida y compararla con las enfermedades priónicas.
Principales métodos:
- Inyección intracerebral de extractos cerebrales diluidos que contienen Abeta de pacientes con EA y ratones transgénicos APP en ratones transgénicos APP.
- Evaluación de la dependencia de tiempo y concentración de la beta-amiloidosis cerebral inducida.
- Evaluar el efecto de la inmunodepleción de Abeta, la desnaturalización de proteínas y la inmunización del huésped en la actividad de siembra.
Principales resultados:
- Los Abeta exógenos de cerebros humanos AD o modelos de ratones transgénicos pueden inducir beta-amiloidosis cerebral y patología asociada en ratones transgénicos APP.
- La amiloidosis inducida demostró una relación dependiente del tiempo y de la concentración.
- La actividad de siembra se redujo significativamente o se eliminó por métodos dirigidos a Abeta, como la inmunodepleción y la inmunización del huésped.
- El fenotipo de amiloidosis resultante varió en función de la fuente del agente de siembra y el huésped, lo que sugiere la existencia de cepas Abeta.
Conclusiones:
- El beta-amiloide exógeno (Abeta) puede actuar como una "semilla" para iniciar la agregación de proteínas y cambios patológicos in vivo, reflejando mecanismos similares a los priones.
- Los hallazgos sugieren la existencia de "cepas" distintas y biológicamente activas de Abeta, que influyen en las características de la patología inducida de la enfermedad de Alzheimer.
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