Researchers are focusing on abnormal proteins that could be causing the brain damage associated with these three neurological diseases.

Is an abnormal protein the cause of Alzheimer’s, Parkinson’s, and Huntington’s diseases?

A group of researchers is looking into that question.

If successful, their research could lead to diagnostic tools and new treatments that could be used on all three of these deadly neurological ailments.

The findings from the scientists at Loyola University Chicago were published late last month in the journal Acta Neuropathologica.

“A possible therapy would involve boosting a brain cell’s ability to degrade a clump of proteins and damage vesicles,” explained Edward Campbell, PhD, study senior author, and an associate professor at Loyola, in a statement. “If we could do this in one disease, it’s a good bet the therapy would be effective in the other two diseases.”

Read more: Get the facts on Alzheimer’s disease »

Neurodegenerative diseases are basically caused by the death of cells in the brain.

In Alzheimer’s, this destruction primarily destroys memory.

In Parkinson’s and Huntington’s, it primarily affects movement.

Despite those effectual differences, the Loyola researchers say they may have discovered a common thread among the trio of diseases.

In all three ailments, previous research has suggested that proteins that are abnormally folded form clumps inside brain cells.

Different proteins have been implicated in each of the three diseases. In Alzheimer’s, it’s tau. In Parkinson’s, it’s alpha-synuclein. In Huntington’s, it’s huntingtin.

The Loyola researchers concluded that these different proteins behave in the same way when they enter brain cells.

They said these proteins invade vesicles, small compartments that are encased in membranes.

The proteins damage those membranes, allowing them to then invade a cell’s cytoplasm and cause even more destruction.

The researchers said the damaged cells try to gather the ruptured vesicles and protein clumps together to destroy them. However, the proteins are resistant to the degradation.

“The cell’s attempt to degrade the proteins is somewhat like a stomach trying to digest a clump of nails,” Campbell said.

Read more: The stages of Parkinson’s disease »

Experts in these fields told Healthline this particular research does provide some encouragement.

James Hendrix, director of global science initiatives at the Alzheimer’s Association, said although the three diseases involve different proteins and have different effects on the brain, there is still some commonality.

He likened it to studying the motors of cars, airplanes, and boats. Although they’re different modes of transport, they still have similar engines.

“It’s valuable to have this cross talk. You don’t want to work in a silo,” Hendrix told Healthline. “A discovery in one area can revolutionize another field.”

George Yohrling, PhD, the senior director of mission and scientific affairs at the Huntington’s Disease Society of America, agrees.

“They’re looking at what’s going on at the cellular level. What cellular machinery is being disrupted,” he told Healthline.

“It gets down to the cellular level,” added Hendrix. “If you can understand what’s going wrong, you might be able to prevent that mechanism from happening.”

A breakthrough is sorely needed for all these diseases.

Late last month, the Centers for Disease Control and Prevention (CDC) announced that the death rate from Alzheimer’s in the United States increased 55 percent between 1999 and 2014.

In addition, about 50,000 people in the United States are diagnosed with Parkinson’s every year. An estimated 500,000 Americans are living with the disease.

Huntington’s usually afflicts people while they are in their 30s and 40s. Most people die 15 to 20 years after diagnosis.

Yohrling and Hendrix both said finding a treatment that worked for all three diseases would be a truly fantastic thing.

“That would be wonderful,” said Yohrling.

“That would be pretty amazing,” added Hendrix.

Read more: Get the facts on Huntington’s disease »