A new study published in the European Journal of Neuroscience has investigated how amyloid-beta pathology in cats with cognitive dysfunction syndrome (CDS) – a naturally occurring condition resembling Alzheimer’s disease (AD) – is linked to synaptic loss through glial activity. The findings suggest parallels between feline dementia and human neurodegenerative disease, highlighting the potential of the feline brain as a comparative model for AD research.
Researchers at the University of Edinburgh examined brain tissue from 25 cats, divided into young, aged, and CDS-affected groups. Brains were examined using immunohistochemistry and confocal microscopy to assess amyloid-beta deposition, synaptic markers, and glial cell activity. Linear mixed-effects modeling was applied to quantify differences between groups.
Analysis showed that amyloid-beta accumulates within synapses in both aged and CDS-affected cats, with no significant difference between these two groups. In regions containing amyloid plaques, microgliosis and astrogliosis were observed, along with increased internalization of amyloid-containing synapses by both microglia and astrocytes.
Notably, microglia appeared more likely than astrocytes to engulf amyloid-positive synapses. Furthermore, in CDS cats – but not in aged cats without clinical dementia – the extent of amyloid burden correlated with glial-mediated synaptic ingestion, suggesting a stronger pathological effect in diseased animals.
The study also points to the potential use of feline CDS as a naturally occurring model for AD. While limited in size, the findings emphasize the importance of distinguishing age-related brain changes from those linked to clinical dementia in diagnostic practice.
The authors note that further research with larger cohorts and advanced imaging will be needed to confirm whether glial-mediated synapse loss is a direct cause of cognitive dysfunction in cats. Still, the evidence supports amyloid-beta pathology as a meaningful marker of disease progression across species.