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Scientists from German Center for Neurodegenerative Diseases have found that the protein medin co-aggregates with amyloid-β in the blood vessels of the brains of Alzheimer’s patients. These findings suggest that medin may play a role in the development of Alzheimer’s disease and may be a potential therapeutic target for the condition.
Previous studies had focused on amyloid-β, but medin had not been a focus of interest because there was little evidence of associated pathology. However, medin is found in the blood vessels of most people over 50 and is the most common amyloid known.
The researchers found that in Alzheimer’s mouse models, medin accumulates even more strongly in the brain’s blood vessels when amyloid-β deposits are also present. These findings were confirmed in brain tissue from organ donors with Alzheimer’s dementia. When mice were genetically modified to prevent medin formation, significantly fewer amyloid-β deposits developed, and there was less damage to blood vessels.

These findings suggest that targeting medin may be a promising approach to preventing the cognitive decline and vascular damage associated with Alzheimer’s disease.