Peer-reviewed veterinary case report
Tau protein changes and brain inflammation linked to dog dementia
By Smolek, Tomas et al.·Published in The Journal of comparative neurology·2016·Institute of Neuroimmunology·View original on PubMed →
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Original publication title: Tau hyperphosphorylation in synaptosomes and neuroinflammation are associated with canine cognitive impairment.
- Species:
- dog
Plain-English summary
A group of older dogs showing signs of cognitive decline, such as memory loss, altered social behavior, and changes in sleep patterns, were examined for brain changes similar to those seen in human Alzheimer's disease. Researchers found that many of these dogs had abnormal protein deposits in their brains, particularly tau proteins, which are linked to cognitive impairment. The study suggests that neuroinflammation and the buildup of these proteins may contribute to the cognitive issues seen in aging dogs. While there is no specific treatment mentioned, understanding these changes can help veterinarians provide better care for dogs with cognitive problems.
People also search for: dog cognitive decline symptoms · older dog memory loss treatment · canine cognitive impairment signs
Abstract
Canine cognitive impairment syndrome (CDS) represents a group of symptoms related to the aging of the canine brain. These changes ultimately lead to a decline of memory function and learning abilities, alteration of social interaction, impairment of normal housetraining, and changes in sleep-wake cycle and general activity. We have clinically examined 215 dogs, 28 of which underwent autopsy. With canine brains, we performed extensive analysis of pathological abnormalities characteristic of human Alzheimer's disease and frontotemporal lobar degeneration, including β-amyloid senile plaques, tau neurofibrillary tangles, and fused in sarcoma (FUS) and TAR DNA-binding protein 43 (TDP43) inclusions. Most demented dogs displayed senile plaques, mainly in the frontal and temporal cortex. Tau neurofibrillary inclusions were found in only one dog. They were identified with antibodies used to detect tau neurofibrillary lesions in the human brain. The inclusions were also positive for Gallyas silver staining. As in humans, they were distributed mainly in the entorhinal cortex, hippocampus, and temporal cortex. On the other hand, FUS and TDP43 aggregates were not present in any of the examined brain samples. We also found that CDS was characterized by the presence of reactive and senescent microglial cells in the frontal cortex. Our transcriptomic study revealed a significant dysregulation of genes involved in neuroinflammation. Finally, we analyzed tau phosphoproteome in the synaptosomes. Proteomic studies revealed a significant increase of hyperphosphorylated tau in synaptosomes of demented dogs compared with nondemented dogs. This study suggests that cognitive decline in dogs is related to the tau synaptic impairment and neuroinflammation. J. Comp. Neurol. 524:874-895, 2016. © 2015 Wiley Periodicals, Inc.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/26239295/