title: Interneurons and beta-amyloid in the olfactory bulb, anterior olfactory nucleus and olfactory tubercle in APPxPS1 transgenic mice model of Alzheimer's disease.
abstract: Impaired olfaction has been described as an early symptom in Alzheimer's disease (AD). Neuroanatomical changes underlying this deficit in the olfactory system are largely unknown. Given that interneuron populations are crucial in olfactory information processing, we have quantitatively analyzed somatostatin- (SOM), parvalbumin- (PV), and calretinin-expressing (CR) cells in the olfactory bulb, anterior olfactory nucleus, and olfactory tubercle in PS1 x APP double transgenic mice model of AD. The experiments were performed in wild type and double transgenic homozygous animal groups of 2, 4, 6, and 8 months of age to analyze early stages of the pathology. In addition, beta-amyloid (Aβ) expression and its correlation with SOM cells have been quantified under confocal microscopy. The results indicate increasing expressions of Aβ with aging as well as an early fall of SOM and CR expression, whereas PV was decreased later in the disease progression. These observations evidence an early, preferential vulnerability of SOM and CR cells in rostral olfactory structures during AD that may be useful to unravel neural basis of olfactory deficits associated to this neurodegenerative disorder.
authors.affiliation: Laboratorio de Neuroplasticidad y Neurodegeneración, Departamento de Ciencias Médicas, Centro Regional de Investigaciones Biomédicas, Facultad de Medicina de Ciudad Real, Universidad de Castilla-La Mancha, 13071 Ciudad Real, Spain.
authors.forename: Daniel
authors.initials: D
authors.lastname: Saiz-Sanchez
authors.forename: Carlos
authors.initials: C
authors.lastname: De La Rosa-Prieto
authors.forename: Isabel
authors.initials: I
authors.lastname: Ubeda-Bañon
authors.forename: Alino
authors.initials: A
authors.lastname: Martinez-Marcos
mesh_terms: D000367:Age Factors; D000544:Alzheimer Disease / Q000235:genetics / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D016564:Amyloid beta-Protein Precursor / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D064032:Calbindin 2 / Q000378:metabolism; D004195:Disease Models, Animal; D018450:Disease Progression; D005260:Female; D006720:Homozygote; D006801:Humans; D007395:Interneurons / Q000378:metabolism* / Q000473:pathology; D051379:Mice; D008822:Mice, Transgenic; D009830:Olfactory Bulb / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D009833:Olfactory Pathways / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D010320:Parvalbumins / Q000378:metabolism; D053764:Presenilin-1 / Q000235:genetics / Q000378:metabolism*; D012903:Smell; D013004:Somatostatin / Q000378:metabolism; D013997:Time Factors
chemical_list: C545487:APP protein, human; D016229:Amyloid beta-Peptides; D016564:Amyloid beta-Protein Precursor; C576511:Calb2 protein, mouse; D064032:Calbindin 2; C508853:PSEN1 protein, human; D010320:Parvalbumins; D053764:Presenilin-1; D013004:Somatostatin
keywords: Alzheimer's disease; amyloid beta; calretinin; olfactory bulb; olfactory deficit; parvalbumin; somatostatin; transgenic mice