How aging cats with dementia reveal Alzheimer’s brain changes

As our understanding of Alzheimer’s disease continues to develop, researchers are increasingly looking beyond traditional models to reveal new insights. A recent study published in European Journal of Neuroscience suggests that older cats with dementia can offer a surprising and valuable window into how Alzheimer’s progressing in the human brain. The results reveal that aging cat brains develop many of the same biological markers associated with Alzheimer’s, including the construction of amyloid beta and disruption of synapses or connections between nerve cells.

This discovery could have consequences for both veterinary and human medicine. The study, led by veterinarian Robert McGeahan at the University of Edinburgh, examined brain tissue after Mortem from 25 cats – seven young and 18 older cats, eight of whom had shown behavioral signs of dementia. Using fluorescent markers to detect amyloid beta, researchers found that older cats, whether they had shown symptoms of dementia, had significantly more amyloid beta deposits than younger cats. In particular, these plaques tend to accumulate near synapses, the compounds themselves that allow nerve cells to communicate effectively.

One of the most compelling aspects of the study is how close the cat pathology reflects the cat pathology seen in Humane Alzheimer’s patients. In both species, the presence of amyloid beta appears to trigger a cascade of immune responses. Microglia, the brain’s immune cells and astrocytes, which help to preserve the brain environment, turned out to be hyperactive in the older cats. These cells were collected near Amyloidplaques and rather than simply clearing the harmful proteins, also seemed to attack the surrounding synapses. This unintended safety injury can be a key factor in the cognitive decline observed in both cats and humans.

I found this detail striking: the immune system’s attempt to protect the brain can actually speed up its deterioration. This double role of microglia and astrocytes – as both protectors and potential aggressors – meets the complexity of our understanding of neurodegenerative diseases. It also opens up new ways of research into how these cells can be modulated to maintain brain function without triggering harmful side effects.

Roberta Marongu, a neuroscientist at Weill Cornell Medicine, who was not involved in the study, noted that these findings are repeating what is observed in Human Alzheimer’s cases. She pointed out that microglia and astrocytes in both humans and cats Sverre around Amyloidplaques and contribute to the degradation of neuronal compounds. This equality strengthens the case to use cats as a natural model for examining Alzheimer’s disease.

Unlike mice often used in Alzheimer’s research and must be genetically modified to develop the condition, cats can develop dementia spontaneously as they grow older. This natural occurrence makes them a potentially more realistic model for examining the progression of the disease. However, the researchers recognize that cats are not without restrictions. They are more expensive to study than mice, and the sample size of this study was relatively small. Yet the parallels between cat and human brain changes are convincing enough to justify further study.

Behaviorally, aging cats with dementia can exhibit symptoms that are far too well -known to those who have cared for people with Alzheimer’s. These may include increased vocalization at night, disturbed sleep patterns and general confusion or disorientation. While these signs alone do not confirm a diagnosis, they are consistent with the biological changes observed in the study, suggesting a strong connection between amyloid beta -building and cognitive decline.

Previous research had identified the presence of amyloid beta in cat brains, but this new study is among the first to investigate how that protein can affect brain function. By focusing on synapses, McGeach and his team were able to highlight a potential mechanism by which cognitive decline occurs. The loss of synaptic compounds is known to be an early feature of Alzheimer’s in humans, and its presence in cats further emphasizes the disease and the range.

The research team plans to expand their study to include more cat brains that can help identify patterns that separate cats with dementia from them without. They are also interested in examining the role of other proteins associated with Alzheimer’s, such as TAU, to see how these markers manifest themselves in cat brains. This broader approach could contribute to a more comprehensive understanding of the disease and potentially lead to new treatment strategies for both cats and humans.

While it is unlikely that cats will replace mice as the primary model of Alzheimer’s research, their spontaneous development of dementia gives a unique opportunity to study the disease in a more natural context. As McGeahan pointed out, the goal is not only to promote human medicine, but also to improve health and quality of life for aging pets. This double advantage makes the study a promising step forward in the ongoing effort to reveal the mysteries of neurodegenerative diseases.

Read more at Sciencenews.org

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