2023-09-21 16:08:00
Every year on September 21, since 1994, World Alzheimer’s Day is celebrated. About 55 million people worldwide suffer from dementia, including Alzheimer’s disease. Two thirds of them live in developing countries. Given the aging population, this number will rise to approximately 139 million by 2050. The number of patients will increase especially sharply in China, India, South America and sub-Saharan Africa.
Researchers around the world have been searching for a cure for Alzheimer’s disease for decades, but have made modest progress so far. Great hopes are placed on the new medical drug Lekanemab. The antibody, approved by the US Food and Drug Administration (FDA) in 2023, may slow the progression of the disease in the early stages.
Complex processes in the brain
The development of effective drugs is complicated by the fact that all the brain processes involved in Alzheimer’s disease have not yet been identified. There is no answer yet to the question of why brain cells die in people with Alzheimer’s disease? Many abnormal proteins, called beta-amyloid and tau proteins, accumulate in the brains of patients with this diagnosis, but the direct connection between these two proteins was previously unclear.
Until now, the connection between amyloid proteins and tau in the brains of Alzheimer’s patients was unclear. Credit: Jens Wolf/dpa/picture-alliance
Cause of cell death revealed
Now Belgian and British researchers believe they have solved the mystery. According to a new study published in the journal Science Magazin, there is a direct link between abnormal proteins that accumulate in the brain and “necroptosis” – a type of cell death.
Typically, necroptosis ensures the removal of unwanted cells and the formation of new ones, especially during immune reactions or inflammatory processes. When the supply of nutrients is depleted, cells swell, thereby destroying their plasma membrane, causing inflammation and cell death.
Brain cells in Alzheimer’s patients become inflamed due to the accumulation of abnormal amyloid in the spaces between neurons, according to a study. This changes the internal chemistry of the cell.
Amyloid clumps together to form so-called “plaques,” and tau protein gathers into bundles of fibers called “tangles.” Thanks to this interaction, brain cells begin to produce the MEG3 molecule. If the research team was able to block MEG3, the brain cells also survived. To do this, the researchers transplanted human brain cells into the brains of genetically modified mice that produce particularly large amounts of abnormal amyloid.
In patients with Alzheimer’s disease, abnormal amyloid accumulates in the spaces between neurons. Photo: National Institute on Aging, NIH/AP/picture alliance
“For the first time, we have gained insight into how and why neurons die in Alzheimer’s disease. There has been a lot of speculation for three to four decades, but no one has been able to pinpoint the mechanisms,” said the scientist involved in the study, led by Professor Bart De Struper from British Dementia Research Institute.
Hopes for new drugs
Researchers from the University of Leuven in Belgium and the UK Dementia Research Institute at University College London hope these new findings will lead to entirely new approaches to developing drugs against Alzheimer’s disease. The hope is not groundless, since a drug such as Lekanemab has recently been developed, which specifically targets the amyloid protein. If you can block the MEG3 molecule with appropriate drugs, you can stop the death of brain cells.
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