Cats showing dementia-like symptoms in later life display changes in their brains strikingly similar to those seen in humans with Alzheimer’s, a new study reveals. Researchers believe this discovery could open doors to fresh avenues of research and potentially accelerate the development of therapies for the notoriously hard-to-treat condition.
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“Progress in treating Alzheimer’s has been fairly limited compared to other diseases,” said Dr Robert McGeachan, lead author of the study, speaking to BBC Science Focus.
“Cats might serve as a more relevant model for the disease because we are observing similar brain changes. By studying Alzheimer’s in cats, we could develop treatments that stand a better chance of working in humans.”
Alzheimer’s, the most common form of dementia, is a collection of neurodegenerative disorders that affect memory, problem-solving, language, and behaviour. Approximately one in nine people over 65 develop the condition, and with ageing populations worldwide, more than 150 million people could be living with Alzheimer’s by 2050. Despite decades of research and billions of dollars spent, effective treatments remain scarce.
It has long been known that cats can exhibit dementia-like symptoms as they grow older. Surveys indicate that nearly a third of cats aged 11 to 14 show at least one sign of feline cognitive dysfunction syndrome (CDS), the veterinary equivalent of dementia. For cats over 15, this figure rises to more than half. Symptoms of feline CDS mirror Alzheimer’s in humans and include disrupted sleep-wake cycles and disorientation. Cats may also become more vocal and seek increased comfort and attention from their owners. Ageing cats’ brains have been observed to accumulate proteins called amyloid-beta plaques, thought to contribute to Alzheimer’s in humans.
“As humans age, these protein plaques can form in the brain, but only some individuals develop Alzheimer’s, and we still don’t fully understand why,” McGeachan explained.
“Previously, we knew older cats developed these proteins and showed signs of dementia, but it was unclear whether the plaques were merely age-related or actively contributing to cognitive decline.”
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To investigate further, McGeachan’s team analysed the brains of 25 cats of varying ages after death, including individuals with CDS symptoms. They discovered that amyloid-beta plaques were not inert. Instead, they were associated with harmful changes, including increased inflammation and glial cells – the brain’s immune cells – engulfing synapses near the plaques.
This research suggests that feline CDS and human Alzheimer’s share not only outward symptoms but also underlying brain mechanisms, positioning cats as a promising model for future studies into dementia treatments.
