Surprising findingsCats might provide breakthrough for Alzheimer's research

RTL Today
This years' August issue of the European Journal of Neuroscience featured a research report regarding a naturally occurring model of Alzheimer's Disease in cats.
© Socreative / Getty Images

As first reported by BBC and Sky News, researchers from the Universities of Edinburgh and California, the UK Dementia Research Institute, and the Scottish Brain Sciences are hopeful as to the breakthrough their work might hold for dementia research.

Funded by Wellcome and the UK Dementia Research Institute, they conducted postmortem brain examinations of 25 cats, eight of which were diagnosed with feline Cognitive Dysfunction Syndrome (CDS) over the course of three months. The CDS-affected cats were compared to two control groups with no prior history of neurological diseases, consisting of seven young cats and 10 aged cats. The latter were age-matched to the CDS group.

CDS is an age-related neurodegenerative disorder similar to dementia in people, characterised by increased vocalisation, for example for increased affection and attention from their owner, altered social interactions and sleep-wake cycles, disorientation, and house-soiling among other symptoms.

In humans, Alzheimer’s usually first targets connections between the parts involving memory, such as the entorhinal cortex and hippocampus, and subsequently affecting areas in the cerebral cortex responsible for language, reasoning, and social behavior.

Although some important characteristics of Alzheimer’s Disease require further investigation in cats to determine common occurrence, others have already been detected in feline dementia such as brain atrophy (loss of brain tissue), neuronal loss, amyloid-beta plaques, tau pathology, and cerebral amyloid angiopathy.

Some levels of amyloid-beta protein naturally occur in healthy ageing. However, these findings of increased amounts of amyloid-beta-containing synapses near plaques found in the cats’ brains are especially significant as they turn fatal for nerve cells on a long-term basis. In human Alzheimer’s, beta-amyloid protein also clumps together to build plaques around nerve cells, thereby disrupting the signal transmission between nerve cells, ultimately causing their decline.

This also suggests that amyloid-beta is in part responsible for mechanisms in both feline and human dementia, which in turn offers valuable insights into the pathogenesis of Alzheimer’s Disease and potential therapeutic targets. These findings are especially relevant because monoclonal antibodies targeting this protein have already exhibited mild success in slowing down cognitive decline in humans and are increasingly approved for treatment globally.

Read the full report here.

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