Journal
ANATOMICAL RECORD-ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY
Volume 296, Issue 9, Pages 1413-1423Publisher
WILEY-BLACKWELL
DOI: 10.1002/ar.22750
Keywords
Alzheimer's disease; amyloid beta; calretinin; olfactory bulb; olfactory deficit; parvalbumin; somatostatin; transgenic mice
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Funding
- Spanish Ministry of Science and Innovation/FEDER [BFU2010-15729]
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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 (A) expression and its correlation with SOM cells have been quantified under confocal microscopy. The results indicate increasing expressions of A 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. (c) 2013 Wiley Periodicals, Inc.
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