Solving the Canine Alzheimer’s Mystery: Uncovering Pathologies in Aging Brains of Dogs

Published on April 27, 2023

Just like humans, aging dogs can develop a condition called Canine Cognitive Dysfunction (CCD) that shares similarities with Alzheimer’s disease. However, little is known about how the brains of dogs age pathologically. In this study, scientists investigated the brains of aged canines and discovered an increase in glial cells and activation of astrocytes, which are indicative of neuroinflammation. They also found an accumulation of two proteins, amyloid beta and hyperphosphorylated tau, in the cortical brain regions of aging dogs. Interestingly, canines with CCD exhibited an additional phosphorylation site on tau at threonine 217, suggesting that this could be a potential predictor for CCD. By unraveling these brain pathologies in aging dogs, researchers are shedding light on the mysteries of canine Alzheimer’s and paving the way for better diagnostics and treatment options for both dogs and humans!

Canine cognitive dysfunction (CCD) syndrome is a well-recognized naturally occurring disease in aged dogs, with a remarkably similar disease course, both in its clinical presentation and neuropathological changes, as humans with Alzheimer’s disease (AD). Similar to human AD patients this naturally occurring disease is found in the aging canine population however, there is little understanding of how the canine brain ages pathologically. It is well known that in neurodegenerative diseases, there is an increase in inflamed glial cells as well as an accumulation of hyperphosphorylation of tau (P-tau) and amyloid beta (Aβ1-42). These pathologies increase neurotoxic signaling and eventual neuronal loss. We assessed these brain pathologies in aged canines and found an increase in the number of glial cells, both astrocytes and microglia, and the activation of astrocytes indicative of neuroinflammation. A rise in the aggregated protein Aβ1-42 and hyperphosphorylated tau, at Threonine 181 and 217, in the cortical brain regions of aging canines. We then asked if any of these aged canines had CCD utilizing the only current diagnostic, owner questionnaires, verifying positive or severe CCD had pathologies of gliosis and accumulation of Aβ1-42 like their aged, matched controls. However uniquely the CCD dogs had P-tau at T217. Therefore, this phosphorylation site of tau at threonine 217 may be a predictor for CCD.

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