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Specific disruption of hippocampal mossy fiber synapses in a mouse model of familial Alzheimer's disease.
Wilke, Scott A; Raam, Tara; Antonios, Joseph K; Bushong, Eric A; Koo, Edward H; Ellisman, Mark H; Ghosh, Anirvan.
Afiliación
  • Wilke SA; Neurobiology Section, Division of Biological Sciences, University of California San Diego, La Jolla, California, United States of America.
  • Raam T; Neurobiology Section, Division of Biological Sciences, University of California San Diego, La Jolla, California, United States of America.
  • Antonios JK; Neurobiology Section, Division of Biological Sciences, University of California San Diego, La Jolla, California, United States of America.
  • Bushong EA; National Center for Microscopy and Imaging Research, University of California San Diego, La Jolla, California, United States of America.
  • Koo EH; Department of Neurosciences, University of California San Diego, La Jolla, California, United States of America.
  • Ellisman MH; National Center for Microscopy and Imaging Research, University of California San Diego, La Jolla, California, United States of America.
  • Ghosh A; Neurobiology Section, Division of Biological Sciences, University of California San Diego, La Jolla, California, United States of America ; Neuroscience Discovery and Translational Area, pRED, F. Hoffmann-La Roche, Basel, Switzerland.
PLoS One ; 9(1): e84349, 2014.
Article en En | MEDLINE | ID: mdl-24454724
The earliest stages of Alzheimer's disease (AD) are characterized by deficits in memory and cognition indicating hippocampal pathology. While it is now recognized that synapse dysfunction precedes the hallmark pathological findings of AD, it is unclear if specific hippocampal synapses are particularly vulnerable. Since the mossy fiber (MF) synapse between dentate gyrus (DG) and CA3 regions underlies critical functions disrupted in AD, we utilized serial block-face electron microscopy (SBEM) to analyze MF microcircuitry in a mouse model of familial Alzheimer's disease (FAD). FAD mutant MF terminal complexes were severely disrupted compared to control - they were smaller, contacted fewer postsynaptic spines and had greater numbers of presynaptic filopodial processes. Multi-headed CA3 dendritic spines in the FAD mutant condition were reduced in complexity and had significantly smaller sites of synaptic contact. Significantly, there was no change in the volume of classical dendritic spines at neighboring inputs to CA3 neurons suggesting input-specific defects in the early course of AD related pathology. These data indicate a specific vulnerability of the DG-CA3 network in AD pathogenesis and demonstrate the utility of SBEM to assess circuit specific alterations in mouse models of human disease.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Sinapsis / Fibras Musgosas del Hipocampo / Enfermedad de Alzheimer Tipo de estudio: Prognostic_studies Límite: Animals / Female / Humans Idioma: En Revista: PLoS One Asunto de la revista: CIENCIA / MEDICINA Año: 2014 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Sinapsis / Fibras Musgosas del Hipocampo / Enfermedad de Alzheimer Tipo de estudio: Prognostic_studies Límite: Animals / Female / Humans Idioma: En Revista: PLoS One Asunto de la revista: CIENCIA / MEDICINA Año: 2014 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos