title: Amyloid-β immunotherapy reduces amyloid plaques and astroglial reaction in aged domestic dogs.
abstract: BACKGROUND
  Alzheimer's disease (AD) is characterized by the dynamic accumulation of extracellular amyloid deposits from the interplay between amyloid-β (Aβ) plaques, reactive astrocytes and activated microglia. Several immunotherapies against Aβ have been shown to reduce amyloid neuropathology. However, the role of the associated glia in the recovery process requires clarification. Previously, we described the safety and effectiveness in aged domestic canine with cognitive dysfunction syndrome of a new active vaccine candidate for the treatment of AD in humans.
  
  
  OBJECTIVE
  The aim of this article is to gain a better understanding of how immunotherapy modifies the amyloid burden and its effects on astroglial and microglial reactivity in immunized dogs.
  
  
  METHODS
  In order to achieve this, we compared and quantified amyloid plaques and astroglial and microglial reactions in the frontal cortex of unimmunized and immunized aged domestic dogs.
  
  
  RESULTS
  We found amyloid plaques from immunized dogs to be smaller and more compact than those from unimmunized dogs. In these new plaques, the associated astrocytes were closer and less immunoreactive to the β subunit of S100 protein (S100B). We also found no modification in the microglial reaction associated with immunization.
  
  
  CONCLUSIONS
  The anti-Aβ immunotherapy developed in our laboratory modifies the equilibrium between soluble and insoluble Aβ in aged dogs in close correlation with S100B-negative astrocytosis and microglial reaction.
authors.affiliation: Unitat de Bioquímica i Biologia Molecular, Facultat de Medicina, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Universitat de Barcelona and Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Barcelona, Spain.
authors.forename: Maria
authors.initials: M
authors.lastname: Neus Bosch
authors.forename: Marco
authors.initials: M
authors.lastname: Pugliese
authors.forename: Carmen
authors.initials: C
authors.lastname: Andrade
authors.forename: Javier
authors.initials: J
authors.lastname: Gimeno-Bayón
authors.forename: Nicole
authors.initials: N
authors.lastname: Mahy
authors.forename: Manuel J
authors.initials: MJ
authors.lastname: Rodriguez
mesh_terms: D000375:Aging / Q000378:metabolism / Q000473:pathology*; D000544:Alzheimer Disease / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control; D016229:Amyloid beta-Peptides / Q000276:immunology* / Q000378:metabolism; D000818:Animals; D001253:Astrocytes / Q000378:metabolism / Q000473:pathology*; D003072:Cognition Disorders / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control; D004195:Disease Models, Animal; D004285:Dogs; D005260:Female; D005625:Frontal Lobe / Q000378:metabolism / Q000473:pathology; D007114:Immunization; D007074:Immunoglobulin G / Q000276:immunology* / Q000494:pharmacology / Q000627:therapeutic use*; D007167:Immunotherapy / Q000379:methods*; D008297:Male; D058225:Plaque, Amyloid / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D064568:S100 Calcium Binding Protein beta Subunit / Q000276:immunology / Q000378:metabolism
chemical_list: D016229:Amyloid beta-Peptides; D007074:Immunoglobulin G; D064568:S100 Calcium Binding Protein beta Subunit