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β‐amyloid cortical deposits are accompanied by the loss of serotonergic neurons in the dog
Author(s) -
Bernedo Vanessa,
Insua Daniel,
Suárez MaríaLuisa,
Santamarina Germán,
Sarasa Manuel,
Pesini Pedro
Publication year - 2009
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.21985
Subject(s) - serotonergic , neurodegeneration , neuroscience , cerebral cortex , pathology , cortex (anatomy) , senile plaques , dementia , biology , alzheimer's disease , medicine , disease , serotonin , receptor
Dogs may naturally suffer an age‐related cognitive impairment that has aroused a great deal of interest, even beyond the field of the veterinary clinic. This canine senile dementia reproduces several key aspects of Alzheimer's disease (AD), including the presence of β‐amyloid (Aβ) deposits in the cerebral cortex, neurodegeneration, and learning and memory impairments. In the present study, we have used unbiased stereological procedures to estimate the number of the dorsal and median raphe nuclei (DRN and MRN, respectively) serotonergic neurons immunolabeled with an anti‐tryptophan hydroxylase (TrH) monoclonal antibody in young and aged dogs without Aβ cortical deposits and in aged dogs with Aβ cortical deposits. The estimated total number of TrH‐labeled neurons (mean ± SD) was 94,790 ± 26,341 for the DRN and 40,404 ± 8,692 for the MRN. The statistical analyses revealed that aged dogs with Aβ cortical pathology had 33% fewer serotonergic neurons in the DRN and MRN than aged dogs without Aβ cortical deposits (108,043 ± 18,800 vs. 162,242 ± 39,942, respectively; P = 0.01). In contrast, no significant variations were found between young and aged dogs without Aβ cortical deposits. These results suggest that degeneration of the serotonergic neurons could be involved in the cognitive damage that accompanies Aβ cortical pathology in the dog and reinforce the use of the canine model for exploring the potential mechanisms linking the cortical Aβ pathology and serotonergic neurodegeneration that occurs during the course of AD. J. Comp. Neurol. 513:417–429, 2009. © 2009 Wiley‐Liss, Inc.