Researchers from the German Center for Neurodegenerative Diseases (DZNE) have discovered that the protein medin co-aggregates with amyloid-β in the blood vessels of the brains of Alzheimer's patients. Their findings were recently published in the prestigious journal Nature. 'Medin has been known
Alzheimer’s disease is a progressive brain disorder that affects memory, thinking, and behavior. It is the most common cause of dementia among older adults and is characterized by the loss of brain cells and the shrinkage of brain tissue. According to the World Health Organization, Alzheimer’s disease affects about 50 million people worldwide, and this number is expected to triple by 2050.
Medin belongs to the group of amyloids. Of these proteins, amyloid-β is best known because it clumps together in the brains of Alzheimer’s patients. These aggregates then deposit both as so-called plaques directly in the brain tissue, but also in its blood vessels, thereby damaging the nerve cells and the blood vessels, respectively. But while many studies have focused on amyloid-β, medin has not been a focus of interest.
“There are only a handful of research groups worldwide working on medin at all,” says Jonas Neher. Most recently, a study from the U.S. reported that medin levels may increase in Alzheimer’s patients. However, it remained unclear whether this increase is merely a consequence of the disease or whether it is one of the causes.
“Amazingly, medin interacts directly with amyloid-β and promotes its aggregation – this was completely unknown,” Jonas Neher summarizes the results.
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