Alzheimer's disease, the leading cause of dementia worldwide, is the focus of much research. A recent study challenges current understanding of this condition.
Until now, scientists believed that Alzheimer's disease was caused by the accumulation of amyloid plaques in the brain, which disrupts communication between cells, activates immune cells, and destroys brain cells.
However, researchers at the Center for Neurodegenerative Disease suggest that beta-amyloid deposits are not solely responsible. They may instead play a supporting role for other proteins, which could be responsible for the damage observed in patients' brain cells. Their study identified more than 20 proteins capable of accumulating with beta-amyloid. Among them, midkine and pleiotrophin even accelerate beta-amyloid aggregation and could play a key role in the development of the disease.
Furthermore, scientists have discovered that more than 30 pathological processes in the body lead to amyloid accumulation. These findings highlight the complexity of brain changes in patients with Alzheimer's disease and could pave the way for new therapeutic strategies.
Pascal Lemontel
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