ArticleThe European journal of neuroscience2025
Amyloid-Beta Pathology Increases Synaptic Engulfment by Glia in Feline Cognitive Dysfunction Syndrome: A Naturally Occurring Model of Alzheimer's Disease.
Article in The European journal of neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- Synaptic vs. Non-Synaptic Glycine Receptors: Physiological Role and Implications in Alzheimer's Disease Pathology.International journal of molecular sciences · 2026Review
- Article
- A Question of Origins: Non-neuronal Sources of Amyloid-β.Neuroscience bulletin · 2026Review
- Cerebral iron deposition in the Globus pallidus and Substantia nigra of aging dogs and cats presenting as bilateral hypointensity on T2w and iron-sensitive MRI sequences (SWI, T2*).Frontiers in veterinary science · 2026Article
- Amyloid-Beta Pathology Increases Synaptic Engulfment by Glia in Feline Cognitive Dysfunction Syndrome: A Naturally Occurring Model of Alzheimer's Disease.The European journal of neuroscience · 2025Article
- Public engagement in translational neuroscience: the good, the bad, and the ugly.Brain communications · 2025Article
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Feline cognitive dysfunction syndrome (CDS; a.k.a. feline dementia) is an age-related neurodegenerative disorder, comparable to dementia in people, characterised by behavioural changes such as increased vocalisation, altered social interactions, sleep-wake cycle, disorientation and house-soiling. Although the underlying mechanisms remain poorly understood, pathologies similar to those observed in Alzheimer's disease (AD) have been identified in the brains of aged or CDS-affected cats, including brain atrophy, neuronal loss, amyloid-beta plaques, tau pathology and cerebral amyloid angiopathy. Neuroinflammation and synapse loss, other important hallmarks of AD, may also play important roles in feline ageing and CDS, but these are yet to be explored. Several mechanisms of synapse loss have been described in human AD and mouse models of amyloidopathy, including synaptic accumulation of amyloid-beta and the aberrant induction of synaptic engulfment by microglia and astrocytes. In this study, immunohistochemistry and confocal microscopy were used to examine the parietal cortex of young (n = 7), aged (n = 10) and CDS-affected (n = 8) cats. Linear mixed effect modelling revealed that amyloid-beta accumulates within synapses in the aged and CDS-affected brain. Additionally, in the aged and CDS groups, there was microgliosis, astrogliosis and increased synaptic engulfment by microglia and astrocytes in regions with Aβ plaques. Further, microglia and astrocytes show increased internalisation of amyloid-beta-containing synapses near plaques. These findings suggest that amyloid-beta exerts a pathogenic effect in the feline brain, with mechanisms mirroring those seen in human AD. Importantly, these results support the use of feline CDS as a naturally occurring, translational model of Alzheimer's disease, offering valuable insights into AD pathogenesis and potential therapeutic targets.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.