A groundbreaking study from Weill Cornell Medicine has revealed that immune cells in the brain, known as border-associated macrophages (BAMs), are responsible for significant blood vessel and tissue damage in patients with the ApoE4 gene variant. This gene increases the risk of Alzheimer’s disease by up to 12-fold and has been linked to vascular dementia, the second-leading cause of cognitive decline.
The research, published in Nature Neuroscience, found that BAMs carrying the ApoE4 variant generate damaging free radicals that impair blood vessels, limiting blood flow essential for brain function and repair. Removing BAMs from models with the ApoE4 variant prevented this damage, highlighting their critical role in the neurodegeneration process.
“These findings help us understand how ApoE4 leads to blood vessel and white matter damage in Alzheimer’s patients,” said study co-senior author Laibaik Park. The study could pave the way for new therapies that target BAMs to reduce the harmful effects of the ApoE4 gene.
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