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Scientists who studied the strongest genetic risk factor for Alzheimer's disease said they have found new evidence on how this factor develops and how its harmful effects on the brain can be reversed.
Doctors have long known that blood vessels in the brain deteriorate with Alzheimer's, especially in people who carry the (APOE4) gene, but the mechanisms behind this have remained unclear.
However, researchers at Icahn School of Medicine at Mount Sinai in New York discovered that the (APOE4) gene damages brain blood vessels and stimulates the accumulation of abnormal proteins.
This occurs by converting cells around blood vessels, which usually stabilize small blood vessels, into scar-forming cells, leading to increased vessel thickness and increased accumulation of misfolded protein clumps known as amyloids, which current treatments target. These conditions can impede blood flow to the brain, leading to damage.
The researchers found that inhibiting a protein called (TGF-beta) involved in tissue cell activity and repair protected the cells around the vessels and reversed the brain vessel degeneration pathway associated with the (APOE4) gene in mice.
The researchers published their findings in two separate research papers in the journals (Cell) and (Cell Stem Cell).
Gil Blanchette, one of the researchers involved in the two research papers, said in a statement that "brain blood vessel damage is not just a late consequence of Alzheimer's; it is a biologically active process caused by APOE4 and may be reversible."
He added, "These findings pave the way for new therapeutic targets to preserve blood vessel function and reduce amyloid accumulation."
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