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It’s long been known that brain vessel dysfunction induced by a peptide called amyloid-beta (Aβ) could lead to Alzheimer’s disease (AD). What’s not known is whether Aβ accumulation is a cause or result of Alzheimer’s. A new study from the University of Mississippi Medical Center in Jackson finds that (Aβ) accumulation in AD is associated with reduced blood flow to the brain, known as cerebral hypoperfusion. This happens by affecting cerebral vascular function via both anterograde (arteriole-to-capillary) and retrograde (capillary-to-arteriole) pathways. These findings provide novel insight into the vascular contribution to AD and lay the groundwork for the development of new treatments for Alzheimer’s.

The team will present their work in person at the American Physiological Society’s (APS) annual meeting at Experimental Biology 2022 in Philadelphia.

AD is the most common form of dementia, mainly affecting people 65 and older. More than 6 million people in the U.S. are living with Alzheimer’s, according to the Alzheimer’s Association. Aβ is a hallmark precursor to AD. This study investigated whether Aβ accumulation induces cerebral hypoperfusion in AD by affecting cerebral vascular function via both anterograde and retrograde pathways. The negative effects of Aβ include vessel constriction and dilation, leading to hypoperfusion.

This study was conducted in a rat model of AD. In addition to the findings above, researchers confirmed that at six months old AD rats displayed cognitive dysfunction in the area of the brain primarily responsible for memory known as the hippocampal region. They also found AD rats displayed impaired response to changes in blood pressure two months earlier than the onset of cognitive deficits.

Our studies give an understanding of how vessel dysfunction could lead to AD and provide critical knowledge for the discovery of new therapeutic strategies to prevent or reverse these devastating diseases.”


Xing Fang, MD, co-author of the study

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