Heterogenous deposition of β-amyloid in the brain of aged dogs

Neurobiol Aging. 2021 Mar:99:44-52. doi: 10.1016/j.neurobiolaging.2020.12.006. Epub 2020 Dec 14.

Abstract

Dogs have been used as animal models for human diseases in which there is beta-amyloid (Aβ) deposition in the central nervous system (CNS), such as Alzheimer's and cerebral amyloid angiopathy (CAA). However, many aspects of Aβ deposition in the CNS of dogs still remain unknown. This study aimed to evaluate the deposition of Aβ in different areas of the CNS of aged dogs from different breeds. Aβ was detected in the brains of aged dogs, forming either senile plaques in the neuropil of cortical gray matter or within the walls of parenchymal or leptomeningeal blood vessels. There was a positive correlation between aging and senile plaques or CAA. In dogs older than 8 years, there was no correlation between the area of Aβ plaques and age, with frontal, temporal, and occipital cortices being affected with approximately equal frequency. There was a positive correlation between Aβ deposition in vessel walls and age. Importantly, CAA was associated with the occurrence of microperivascular hemorrhages in the brains of aged dogs. In conclusion, this study demonstrated that Aβ deposition as plaques or within vessel walls are extremely heterogenous in dogs from different breeds and sizes. Although many features of this disease in dogs are similar to those observed in humans, the choice of dog breed and size as a model for human disease will substantially affect the pattern of Aβ deposition.

Keywords: Aging; Alzheimer's; Aβ; Cerebral amyloid angiopathy; Neuropathology; Senile plaques.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aging / metabolism*
  • Alzheimer Disease / etiology
  • Amyloid beta-Peptides / metabolism*
  • Animals
  • Blood Vessels / metabolism
  • Body Size*
  • Brain / blood supply
  • Brain / metabolism*
  • Cerebral Amyloid Angiopathy / etiology
  • Disease Models, Animal*
  • Dogs*
  • Plaque, Amyloid / metabolism

Substances

  • Amyloid beta-Peptides