Study indicates a vascular link to Alzheimer’s

Studies have shown a link between Alzheimer's disease and a gene called ApoE4. People who carry two copies of the gene have approximately 8 to 10 times the risk of getting Alzheimer's than those who do not have the gene.

Little has been known about how ApoE4 contributes to Alzheimer's deterioration of the brain. However, in a study published in "Nature," scientists from Rochester University and the University of Southern California have shown how ApoE4 can unleash an excess of the protein cyclophilin A into the cardiovascular system, causing inflammation in atherosclerosis and other conditions. The study also found that ApoE4 makes it more likely for cyclophilin A to accumulate in cells that help maintain the blood-brain barrier, reducing blood to the brain and allowing toxic substances to infiltrate.

"We are beginning to understand much more about how ApoE4 may be contributing to Alzheimer's disease," Dr. Robert Bell of Rochester University and senior author of the study, said in a statement. "In the presence of ApoE4, increased cyclophilin A causes a breakdown of cells lining the blood vessels in the brain in the same way as found in cardiovascular disease or abdominal aneurysm.This establishes a new vascular target to fight Alzheimer's disease."

For years, amyloid beta, a protein that accumulates in the brains of Alzheimer patients has been seen as the main culprit for damage. However, this recent study shows that there is also a serious vascular origin, according to the authors. "Our study has shown major neuronal injury resulting from vascular defects that are not related to amyloid beta," Dr. Berislav Zlokovic, an adjunct professor at Rochester and director of the Center for Neurodegeneration and Regeneration, said in a statement. "This damage results from a breakdown of the blood-brain barrier and a reduction in blood flow. Amyloid beta has an important role in Alzheimer's disease," Zlokovic said. "But it's very important to investigate other leads, perhaps where amyloid beta isn't as centrally involved."

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