Toxic protein clumps damage brain blood vessels in Parkinson’s: Study

Along with neurodegeneration, vascular issues may drive disease progression

• Parkinson's disease involves toxic alpha-synuclein protein clumps damaging both brain cells and blood vessels.
• These clumps weaken blood vessel lining, disrupt the blood-brain barrier, and impair blood flow.
• New 3D lab models and AI aim to develop treatments targeting both neuronal and vascular damage.

In Parkinson’s disease, toxic clumps of alpha-synuclein protein not only damage brain cells but also weaken the lining of blood vessels, with both processes likely working together to drive disease progression, according to a study by researchers from Binghamton University in New York and Drexel University in Philadelphia.

“Parkinson’s is a multifaceted disease,” Jungwook “Jay” Paek, PhD, an assistant professor in Binghamton University’s department of electrical and computer engineering, said in a Binghamton University press release. “Understanding the complex interplay between neurodegeneration and vascular pathology [disease-causing mechanisms] offers unique opportunities to help patients.”

The study, “Microengineering of the capillary interface of midbrain dopaminergic neurons to study Parkinson’s disease vascular alterations,” was published in Communications Engineering.

New findings shed light on vascular complications

Parkinson’s disease causes the loss of dopaminergic neurons, the nerve cells in the brain that produce dopamine, a chemical needed for motor control. Research has long focused on this loss of dopaminergic neurons, but there are also problems with brain blood vessels that are less well understood.

One hallmark of Parkinson’s is the buildup of alpha-synuclein. Normally, this protein helps nerve cells function, but in Parkinson’s, it can misfold and clump into toxic aggregates that damage dopaminergic neurons. Now, the researchers found that they can also damage the blood vessels that supply the brain with oxygen and nutrients through the protective layer called the blood–brain barrier.

“Before this research, most studies on Parkinson’s disease have focused on the aggregation of specific proteins and their impacts on neurodegeneration,” Paek said. “However, how the protein aggregation contributes to vascular complications remains largely underexplored, so this is an exciting finding.”