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Interneurons and Beta‐Amyloid in the Olfactory Bulb, Anterior Olfactory Nucleus and Olfactory Tubercle in APPxPS1 Transgenic Mice Model of Alzheimer's Disease
Author(s) -
SaizSanchez Daniel,
De La RosaPrieto Carlos,
UbedaBañon Isabel,
MartinezMarcos Alino
Publication year - 2013
Publication title -
the anatomical record
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.678
H-Index - 62
eISSN - 1932-8494
pISSN - 1932-8486
DOI - 10.1002/ar.22750
Subject(s) - anterior olfactory nucleus , olfactory bulb , olfactory tubercle , calretinin , olfactory system , neuroscience , olfaction , biology , amygdala , olfactory marker protein , genetically modified mouse , olfactory ensheathing glia , pathology , central nervous system , transgene , medicine , immunohistochemistry , immunology , biochemistry , gene
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. Anat Rec, 296:1413‐1423, 2013. © 2013 Wiley Periodicals, Inc.