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You are at:Home»News»Neuropathological basis of visual dysfunction in rare Alzheimer’s forms
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Neuropathological basis of visual dysfunction in rare Alzheimer’s forms

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Differences in the distribution of certain proteins and markers in the brain can explain why some people first experience vision changes instead of memory loss in Alzheimer’s disease, finds a new study by UCL researchers.

Posterior cortical atrophy (PCA) is a rare form of Alzheimer’s disease that, instead of causing memory problems, leads to problems with reading, navigating and recognizing objects. Studies suggest that one in 10 patients with Alzheimer’s disease has a form that is visual, instead of memory LED.

In addition to presenting unusual symptoms, people with PCA usually develop symptoms that are younger than most people with Alzheimer’s disease, usually in the 50s and 60s.

In a new study, published in Neuropathology and applied neurobiology And supported by the society of Alzheimer’s, researchers studied brain tissues of 26 people with PCA and 27 people with typical Alzheimer’s disease who had donated their brains for research at the Queen Square Brain Bank at UCL.

The researchers looked at specific proteins and markers in different parts of the brain to see how they were influenced.

They measure the quantity and distribution of amyloid and tau (proteins related to Alzheimer’s disease) and microglia (an important part of the brain immune system involved in cleaning up damaged brain cells and proteins).

The study showed that in people with PCA the distribution of amyloid and Tau was more widespread at the back of the brain (the parietal region), where visual information is processed and integrated.

They also discovered that microglial activity in PCA was increased, in particular in brain areas that are typically vulnerable to Alzheimer’s disease, for example the sides of the brain (temporary areas), the part of the brain that are characteristic vulnerable in typical memory-led Alzheimer’s disease.

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The temporary area of ​​patients with more typical memory, on the other hand, had the lowest amount of microglial activity and the highest amount of Tau compared to other brain areas.

This shows how the distribution of certain proteins and markers associated with Alzheimer’s disease can lead to various symptoms.

Main author, Dr. Zeinab Abdi (UCL Queen Square Institute of Neurology) said: “These findings suggest that there is a connection between the location of inflammation and accumulation of the proteins associated with Alzheimer’s disease, which can explain why some people get memorial symptoms, while others have problems with vision.”

The researchers hope that their findings will stimulate future research into the relationship between inflammation and accumulation of brain proteins in Alzheimer’s disease and ultimately lead to targeted treatments and more tailor -made care for the patients of Alzheimer’s.

By understanding the unique characteristics of rare, visual forms of Alzheimer’s disease, we can get closer to the development of targeted treatments that meet the specific needs of each patient. This research emphasizes the importance of personalized approaches in tackling this complex disease. “

Dr. Zeinab Abdi, Queen Square Institute of Neurology, University College London

Dr. Richard Oakley, Alzheimer’s Society Associate Director of Research and Innovation, said: “Dementia is the biggest murderer of the UK, with about a million people with the condition. It is a very complex disease and we need to know more about what it causes, so we can beat it.

“There is much that we do not yet understand about rarer and atypical forms of dementia. Without understanding the mechanisms that underlie these less common forms of Alzheimer’s disease, we cannot develop accurate ways to diagnose or treat these diseases.

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“That is why Alzheimer’s society is proud to finance studies such as this, which take a step forward in the complexity of a rare variant of Alzheimer’s disease – revealing how protein accumulation and inflammation vary in brain areas compared to more typical forms of the disease.

“This type of work is crucial to bring us close to a better diagnosis and new treatments, so that no one is left behind, regardless of what kind of dementia they have.

“Research will beat dementia and therefore Alzheimer’s Society finances more than £ 53 million in research and supports more than 400 researchers in the United Kingdom. Discover more on Alzheimers.org.uk/research.”

Source:

University College London

Alzheimers basis dysfunction forms Neuropathological rare visual
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