Cats who develop dementia-like symptoms in old age have similar changes in their brain to humans with Alzheimer’s, a new study has found. The findings could kick down the door to new research, possibly helping fuel the discovery of therapies for the notoriously difficult-to-treat disease.
“Compared to other diseases, our progress in treating Alzheimer’s has been fairly poor,” Dr Robert McGeachan, lead author of the new study, told BBC Science Focus.
“Cats could be a better, more relevant model for the disease because we’re seeing similar things happening in the brain. By studying Alzheimer’s in cats, we can perhaps develop treatments that are more likely to be successful in humans.”
Alzheimer’s is the most common form of dementia, a collection of neurodegenerative diseases affecting people’s memory, problem-solving, language and behaviour. Roughly 1 in 9 people aged over 65 has Alzheimer’s, and with global populations ageing, more than 150 million people could be living with the disease by 2050.
Yet despite decades of research and billions of dollars spent, almost no effective treatments are available today.
How cats get dementia
The knowledge that cats exhibit dementia-like symptoms as they age is not new. According to one survey, nearly a third of cats aged 11 to 14 exhibit at least one sign of feline cognitive dysfunction syndrome (CDS) – the veterinary term for the cat equivalent of dementia. For cats over 15, that figure jumps to more than half.
Symptoms of feline CDS, much like Alzheimer’s, include changes in the sleep-wake cycle and disorientation. Cats may also become more vocal (meowing more) and often desire more comfort and attention from their owners.
As is the case with older humans, it was also known that the brains of ageing cats were often covered in accumulations of proteins, known as ‘amyloid-beta plaques’, which are thought to contribute to the development of Alzheimer’s.
“As they age, humans develop these protein plaques in the brain. But only some people get Alzheimer’s, and we still don’t really know why,” McGeachan said.
“That’s where we were with cats. We knew they got dementia, and we knew that as they aged, some developed these proteins in the brain. Yet we didn’t know whether this was just age-related or whether it could be contributing to the dementia.”
To find out more, McGeachan’s team examined the brains of 25 cats of different ages after they had died, including those with symptoms of CDS.
The researchers found that amyloid-beta plaques weren’t just sitting passively in the brain but were linked with harmful changes. Around the protein plaques, they observed increased inflammation and evidence that glial cells – the immune cells of the brain – were “engulfing” synapses.
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Synapses are the tiny junctions that allow brain cells to communicate, and it is their gradual loss that neuroscientists believe underlies many of the memory and behavioural symptoms of dementia.
The results suggest that the same toxic chain reaction may be occurring in cats: as amyloid-beta builds up, glial cells become activated and consume healthy synapses. But while this broad pattern was clear, the finer detail turned out to be more complicated.
When the researchers compared brains across the different age groups, they found a nuanced picture. Cats with dementia looked very different from young cats, with more amyloid plaques, inflammation and synapse loss. But surprisingly, they didn’t look dramatically different from older, but otherwise healthy, cats.
This meant the researchers couldn’t find a clear dividing line between simply being old and having dementia.
However, there was a hidden difference when the team looked at the relationship between amyloid plaques and synaptic engulfment. In healthy older cats, having more amyloid didn’t necessarily mean more damage. But in cats with dementia, it did: the more plaques they had, the more inflammation and brain-cell loss they showed.
McGeachan thinks this mirrors the situation in people. Many older humans accumulate amyloid plaques in their brains without ever developing Alzheimer’s, while others go on to suffer severe memory decline.
“It may be that the amyloids are having more toxic effects in cats with CDS,” he said. “It could be inducing more inflammation and synaptic engulfment, and that’s why we see a correlation with amyloid in the dementia group and not in the aged group.”
In other words, amyloid build-up may play a role in dementia in cats, but they may not tell the whole story. Just as in human Alzheimer’s, the condition is likely caused by a messy interplay of several factors.
Why cats matter
Alzheimer’s studies have traditionally relied on rodents, where the disease has to be engineered artificially by tweaking genes.
While these models are useful for probing molecular pathways, they often fail to capture the complexity of a naturally occurring disease that unfolds over decades. As a result, countless promising drugs have cleared mouse trials only to fail in human patients.
Cats, however, develop dementia spontaneously as part of ageing in a way that looks remarkably similar to the human condition. What’s more, they live in the same environments as us, sharing many of the same risk factors, from diet to air quality.
This makes them a far more realistic model for unpicking not only the biology of the disease but also the environmental triggers that may push some individuals over the edge.
“Cats could be a stepping stone towards us trying to find treatments that would actually be effective,” McGeachan said.
Next steps
For now, the results raise as many questions as they answer. The study was based on just 25 cats, so a larger sample size may be needed to “tease out the exact mechanisms which are causing the clinical results,” McGeachan said.
Another priority is tau. Alongside amyloid-beta, tau is the other hallmark protein of Alzheimer’s disease. But instead of forming plaques outside brain cells, tau is a protein that twists into tangles inside them. In humans, many researchers believe tau is what drives the most devastating stages of the disease, yet the new cat study did not examine it.
Not to be left out, dogs may also provide another promising avenue. Like cats, they can develop dementia-like syndromes as they age, with symptoms familiar to many owners: disrupted sleep, anxiety, and forgetfulness. Comparing canine and feline brains could reveal whether the same biological processes are at play across species.
Ultimately, this line of research doesn’t just promise insights for human medicine.
“Feline dementia is so distressing for the cat and for its person,” said Prof Danièlle Gunn-Moore, co-author of the study and personal chair of Feline Medicine at the Royal (Dick) School of Veterinary Studies.
“It is by undertaking studies like this that we will understand how best to treat them. This will be wonderful for the cats, their owners, people with Alzheimer’s and their loved ones. Feline dementia is the perfect natural model for Alzheimer’s; everyone benefits.”
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About our expert
Robert McGeachan is a resident in veterinary neurology and neurosurgery, and ECAT veterinary clinical lecturer at the University of Edinburgh, UK. His research has been published in journals such as the European Journal of Neuroscience, Scientific Reports and Nature Neuroscience.