Introduction
Alzheimer’s disease (AD), both in humans and dogs, involves complex neurodegenerative changes. Understanding their similarities and differences improves treatment and expands understanding of the disease.
Detailed Evidence and Analysis
1. Accumulation of Beta-Amyloid and Plaque Formation: In both humans and dogs, beta-amyloid peptide accumulates in the brain, leading to the formation of plaques. In dogs, these plaques tend to be diffuse and are common in the prefrontal cortex and hippocampus. In humans, in addition to diffuse plaques, neuritic plaques and neurofibrillary tangles develop, something rare in dogs (HEAD et al., 2010).
2. Structural and Cognitive Changes: Dogs with Canine Cognitive Dysfunction (CHD) show progressive cognitive decline, similar to early dementia in human Alzheimer’s. It has been observed that beta-amyloid accumulation is correlated with cognitive decline in dogs, even in the absence of neurofibrillary tangles (CUMMINGS et al., 1996).
3. Tauopathies and Tau Hypophosphorylation: Unlike humans, dogs with CHD generally do not present tau neurofibrillary tangles. However, increased hyperphosphorylated tau has been observed in dogs, indicating some level of tau dysfunction (ABEY et al., 2020).
4. Genetics and Transgenic Models: Transgenic dog models have been used to study human genetic mutations related to Alzheimer’s, offering valuable insights into the disease (LEE et al., 2014).
5. Influence of Oxidative Stress: Oxidative stress contributes to brain degeneration in dogs, in a similar way to human Alzheimer’s, pointing to the relevance of the canine model in the study of this disease (ROMANUCCI & DELLA SALDA, 2015).
6. Gut-Brain Axis: Changes in the intestinal microbiome and their connection with Alzheimer’s are being investigated in humans and dogs, highlighting the importance of the gut-brain axis in neurodegenerative diseases (AMBROSINI et al., 2019).
Conclusion
Comparison of canine and human Alzheimer’s reveals striking similarities in beta-amyloid accumulation and cognitive changes, but significant differences in tau pathology and genetics. These findings highlight the importance of dogs as models for studying Alzheimer’s, contributing to better understanding and more effective therapeutic approaches.
References
• HEAD, E. et al. Amyloid-beta peptide and oligomers in the brain and cerebrospinal fluid of aged canines. Journal of Alzheimer’s Disease, vol. 20, no. 2, p. 637-646, 2010.
• CUMMINGS, BJ et al. The canine as an animal model of human aging and dementia. Neurobiology of Aging, vol. 17, p. 259-268, 1996. • ABEY, A. et al. Distribution of tau hyperphosphorylation in canine dementia resembles early Alzheimer’s disease and other tauopathies. Brain Pathology, vol. 31, p. 144-162, 2020.
• LEE, G.-S. et al. A canine model of Alzheimer’s disease generated by overexpressing a mutated human amyloid precursor protein. International Journal of Molecular Medicine, vol. 33, no. 4, p. 1003-1012, 2014.
• ROMANUCCI, M.; DELLA SALDA, L. Oxidative Stress and Protein Quality Control Systems in the Aged Canine Brain as a Model for Human Neurodegenerative Disorders. Oxidative Medicine and Cellular Longevity, vol. 2015, 2015.
• AMBROSINI, Y. et al. The Gut-Brain Axis in Neurodegenerative Diseases and Relevance of the Canine Model: A Review. Frontiers in Aging Neuroscience, vol. 11, 2019.
