Initial findings of Alzheimer's have led to a discovery that it only affects the brain cells. The disease results from a plaque formed by an Amyloid-beta protein, which damages brain cells. However, recent studies have shown that blood vessels are also affected, but reasons are yet to be discovered. It was revealed that blood vessels in the brain undergo changes that may be utilized as a path for new drugs to treat the disease.

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The study is led by a team of researchers from the University of Manchester. Their findings are published in an online journal, Proceedings of the National Academy of Sciences. According to the team's investigation, a smaller version of the protein called Amyloid-β 1-40 clogs the small arteries, which causes irregular blood flow. Due to plaque formation, the brain cannot receive sufficient nutrients to function well. The small arteries that allow blood flow are called pial arteries. These arteries are found on the brain's surface, which controls blood and oxygen supply. Insufficient blood and oxygen in the brain lead to memory loss.

"To date, over 500 drugs have been trialed as a cure for Alzheimer's disease. All of them have targeted the nerves in the brain, and none of them have been successful. By showing exactly how Alzheimer's disease affects the small blood vessels, we have opened the door to new avenues of research to find an effective treatment," Dr. Adam Greenstein shared. He is the study's lead researcher and a Clinical Senior Lecturer in Cardiovascular Sciences at the University of Manchester.

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Older mice were the subject of their study. After conducting observations, the team found out that mice with Alzheimer's with too much Aβ1-40 have narrower pial arteries than healthy mice. The narrowing of arteries is caused by Aβ 1-40 switching off a protein called BK in cells lining blood vessels. A BK normally functions when it signals the arteries to widen. The data was gathered by an experiment including BK and Aβ 1-40. Researchers exposed healthy pial arteries for one hour in Aβ 1-40 and then measured signals brought by BK protein. Afterward, it was confirmed that Aβ 1-40 weakened the signals that led to narrowed blood vessels.

"This research is an important step forward in our understanding of Alzheimer's disease. More than half a million people in the UK are living with the condition, and that number is set to rise as our population gets older. These findings could lead to a desperately needed treatment for this devastating condition," says Professor Metin Avkiran, Associate Medical Director at the British Heart Foundation. The team is now finding out which part of Aβ 1-40 damages BK protein. These discoveries will be the foundation of newly developed drugs that could help prevent people from acquiring Alzheimer's.