VIII Conferencia Bienal
Barcelona/Pittsburgh
La demencia hoy23-25 Mayo 2012
VIII Barcelona/Pittsburgh
Biennial Conference
Dementia today23TH-25TH May 2012
Próxima edición de la Conferencia Barcelona-Pittsburgh: 23-25 Mayo 2012 - Next edition of the Barcelona/Pittsburgh Conference 23th-25th May 2012.

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Agenda

Charla "La memoria y la atención. Cambios en la edad adulta" - Jornadas de Puertas Abiertas - Fundació ACE. Institut Català de Neurociències Aplicades

Fecha
22-09-2011 al 22-09-2011

Lugar
Centro Cívico Cotxeres de Sants - Barcelona - España

Organizado por
Fundació ACE. Institut Català de Neurociències Aplicades

Más información

Charla "Tipos de memoria y por qué se afectan"- "La respuesta social ante la demencia" - Jornadas de Puertas Abiertas - Fundació ACE. Institut Català de Neurociències Aplicades

Fecha
13-09-2011 al 13-09-2011

Lugar
Centro Cívico Can Deu - Barcelona - España

Organizado por
Fundació ACE. Institut Català de Neurociències Aplicades

Más información

"Ageing and Neurodegeneration"

Fecha
01-09-2011 al 04-09-2011

Lugar
Bergisch Gladbach - Alemania

Organizado por
DZNE, the German Center for Neurodegenerative Diseases and the Max Planck Institute for Biology of Ageing

Más información



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Persistent Amyloidosis following Suppression of Aâ Production in a Transgenic Model of Alzheimer Disease

Joanna L. Jankowsky, Hilda H. Slunt, Victoria Gonzales, Alena V. Savonenko, Jason C. Wen, Nancy A. Jenkins, Neal G. Copeland, Linda H. Younkin, Henry A. Lester, Steven G. Younkin, David R. Borchelt

Plos Medicine, Plos Medicine Volume 2; Issue 12; December 2005

Año: 2005

Categoría: Investigación Alzheimer

Abstract
Background
The proteases (secretases) that cleave amyloid-â (Aâ) peptide from the amyloid precursor protein (APP) have been the focus of considerable investigation in the development of treatments for Alzheimer disease. The prediction has been that reducing Aâ production in the brain, even after the onset of clinical symptoms and the development of associated pathology, will facilitate the repair of damaged tissue and removal of amyloid lesions. However, no long-term studies using animal models of amyloid pathology have yet been performed to test this hypothesis.

Methods and Findings
We have generated a transgenic mouse model that genetically mimics the arrest of Aâ production expected from treatment with secretase inhibitors. These mice overexpress mutant APP from a vector that can be regulated by doxycycline. Under normal conditions, high-level expression of APP quickly induces fulminant amyloid pathology. We show that doxycycline administration inhibits transgenic APP expression by greater than 95% and reduces Aâ production to levels found in nontransgenic mice. Suppression of transgenic Aâ synthesis in this model abruptly halts the progression of amyloid pathology. However, formation and disaggregation of amyloid deposits appear to be in disequilibrium as the plaques require far longer to disperse than to assemble. Mice in which APP synthesis was suppressed for as long as 6 mo after the formation of Aâ deposits retain a considerable amyloid load, with little sign of active clearance.

Conclusion
This study demonstrates that amyloid lesions in transgenic mice are highly stable structures in vivo that are slow to disaggregate. Our findings suggest that arresting Aâ production in patients with Alzheimer disease should halt the progression of pathology, but that early treatment may be imperative, as it appears that amyloid deposits, once formed, will require additional intervention to clear.

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