Restoring missing lipid may help ease dementia damage in brain, study finds

• Researchers have discovered a new way that brain blood flow problems are connected to a particular type of dementia called vascular dementia.
• They found that a protein called Piezo1 stops working properly due to the loss of a certain fat (PIP₂).
• Fixing this, they found, can help restore normal blood flow in early tests, which could become a new treatment for dementia.

Vascular dementia is a type of dementia that causes changes in memory, thinking, and behavior that result from conditions that affect the blood vessels in the brain. A person’s cognition and brain function can be greatly affected by the size, location, and number of vascular changes. It can occur alone or be part of a diagnosis of Alzheimer’s disease or other forms of dementia.

A recent study published in Proceedings of the National Academy of Sciences provided insights into the biological mechanisms that regulate blood flow in the brain and suggested a possible therapeutic strategy to correct vascular dysfunction.

These preclinical findings showed that adding a missing phospholipid (fat) back into the bloodstream might help improve blood flow and reduce the symptoms of dementia.

Osama Harraz, PhD, researcher on the study and Bloomfield Professor in Cardiovascular Research, assistant professor of pharmacology at the Larner College of Medicine at the University of Vermont, explained their findings to Medical News Today:

“Our findings highlight a previously unknown, targetable mechanism that links impaired brain blood flow to dementia. We identified dysregulation of a protein (Piezo1) in the brain vasculature as a common feature across conditions associated with reduced brain blood flow. Importantly, we show that this dysfunction is driven by loss of a specific regulatory pathway involving a phospholipid (PIP₂), and that restoring this regulation can reverse blood-flow abnormalities in preclinical models.”

Why these findings are important

“These results shift attention toward neurovascular mechanisms as critical drivers of cognitive decline, rather than passive consequences of neurodegeneration. From a therapeutic standpoint, we suggest that normalizing vascular signaling could represent a new strategy to prevent or slow dementia progression, particularly in forms where vascular dysfunction plays a prominent role.”
— Osama Harraz, PhD