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This work was supported by the Spanish Ministry of Economy and Competitiveness (SAF-2014-53040-P (Jesus Avila) and RYC-2015-17189 (Maria Llorens-Martin)); the Centro de Investigacion Biome dica en Red sobre Enfermedades Neurodegenerativas (CIBERNED, Spain) (Jesus Avila); the Alzheimer's Association (2015-NIRG-340709 (Maria Llorens-Martin)); and the Association for Frontotemporal Degeneration (2016 Basic Science Pilot Grant Award (Maria Llorens-Martin)). These funding sources had no involvement in the design of the experiments, analysis of the data or manuscript preparation. Institutional grants from the Fundacion Ramon Areces and Banco de Santander to the CBMSO are also acknowledged.

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Untold New Beginnings: Adult Hippocampal Neurogenesis and Alzheimer's Disease

Publicado en:Journal Of Alzheimer's Disease. 64 (s1): S497-S505 - 2018-01-01 64(s1), DOI: 10.3233/JAD-179918

Autores: Teixeira, Catia M.; Pallas-Bazarra, Noemi; Bolos, Marta; Terreros-Roncal, Julia; Avila, Jesus; Llorens-Martin, Maria;

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Resumen

Neurogenesis occurs in a limited number of brain regions during adulthood. Of these, the hippocampus has attracted great interest due to its involvement in memory processing. Moreover, both the hippocampus and the main area that innervates this structure, namely the entorhinal cortex, show remarkable atrophy in patients with Alzheimer's disease (AD). Adult hippocampal neurogenesis is a process that continuously gives rise to newborn granule neurons in the dentate gyrus. These cells coexist with developmentally generated granule neurons in this structure, and both cooperative and competition phenomena regulate the communication between these two types of cells. Importantly, it has been revealed that GSK-3 beta and tau proteins, which are two of the main players driving AD pathology, are cornerstones of adult hippocampal neurogenesis regulation. We have shown that alterations either promoting or impeding the actions of these two proteins have detrimental effects on the structural plasticity of granule neurons. Of note, these impairments occur both under basal conditions and in response to detrimental and neuroprotective stimuli. Thus, in order to achieve the full effectiveness of future therapies for AD, we propose that attention be turned toward identifying the pathological and physiological actions of the proteins involved in the pathogenesis of this condition.

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