Effect of aging on neurogenesis in the canine brain |
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Authors: | Pekcec Anton Baumgärtner Wolfgang Bankstahl Jens P Stein Veronika M Potschka Heidrun |
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Institution: | Department of Pharmacology, Toxicology, and Pharmacy, Ludwig-Maximilians-University, Munich, Germany; Center for Systems Neuroscience, Hannover, Germany; Department of Pathology, University of Veterinary Medicine, Hannover, Germany; Department of Pharmacology, Toxicology, and Pharmacy, University of Veterinary Medicine, Hannover, Germany; Department of Small Animal Medicine and Surgery, University of Veterinary Medicine, Hannover, Germany |
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Abstract: | An age-dependent decline in hippocampal neurogenesis has been reported in laboratory rodents. Environmental enrichment proved to be a strong trigger of neurogenesis in young and aged laboratory rodents, which are generally kept in facilities with a paucity of environmental stimuli. These data raise the question whether an age-dependent decline in hippocampal cell proliferation and neurogenesis can also be observed in individuals exposed to diversified and varying surroundings. Therefore, we determined rates of canine hippocampal neurogenesis using post-mortem tissue from 37 nonlaboratory dogs that were exposed to a variety of environmental conditions throughout their life. Expression of the neuronal progenitor cell marker doublecortin clearly correlated with age. The analysis of doublecortin-labeled cells in dogs aged > 133 months indicated a 96% drop in the aged canine brain as compared to young adults. Expression of the proliferation marker Ki-67 in the subgranular zone decreased until dogs were aged 85-132 months. In the aging canine brain amyloid-beta peptide deposits have been described that might resemble an early pathophysiological change in the course of human Alzheimer's disease. Comparison of Ki-67 and doublecortin expression in canine brain tissue with or without diffuse plaques revealed no differences. The data indicate that occurrence of diffuse plaques in the aging brain is not sufficient to trigger enhanced proliferation or enhanced neurogenesis such as described in human Alzheimer's disease. In addition, this study gives first proof that an age-dependent decline also dominates hippocampal neurogenesis rates in individuals living in diversified environments. |
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Keywords: | aging Alzheimer's disease doublecortin Ki-67 neurogenesis neuronal progenitor |
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