The Relation between canine cognitive dysfunction and age-related brain lesions.

Area of Science:

• Veterinary Neurology
• Animal Pathology
• Neuroscience

Background:

• Canine cognitive dysfunction (CCD) presents with behavioral changes like disorientation.
• Beta-amyloid deposition (senile plaques and cerebral amyloid angiopathy) is a suspected cause of CCD.
• The exact role of beta-amyloid in CCD pathogenesis remains unclear.

Purpose of the Study:

• To investigate the correlation between age-related brain histopathological lesions and CCD clinical symptoms in dogs.
• To clarify the pathological significance of beta-amyloid deposition in canine cognitive dysfunction.

Main Methods:

• Assessed beta-amyloid deposition (SP and CAA), ubiquitin-positive granules (UBQ), astrocytes (GFAP), microglia (Iba-1), and neurons (Nissl stain) in canine brains.
• Evaluated CCD symptoms using a validated questionnaire in dogs aged 10+ years.
• Analyzed histopathological lesions in 37 aged dogs and correlated findings with CCD scores.

Main Results:

• No significant correlation was found between senile plaque (SP) severity and CCD.
• Cerebral amyloid angiopathy (CAA) increased with age but showed weak correlation with CCD scores.
• Increased ubiquitin (UBQ), astrocytes, and microglia significantly correlated with CCD severity.

Conclusions:

• Beta-amyloid deposition, particularly SP, is not a direct pathogenic factor in canine cognitive dysfunction.
• Synaptic and/or myelin impairment, suggested by increased UBQ and glial activation, may play a role in CCD pathogenesis.
• Glial cell activation and synaptic changes are more strongly associated with CCD than beta-amyloid accumulation.