Alzheimer's Breakthrough May 'Rescue' Early Neuron Loss

Scientists have identified a potential new target for treating Alzheimer's and other neurodegenerative diseases. The discovery promises to halt or even reverse the disease process.

Alzheimer's disease affects roughly 5.8 million Americans, according to the Centers for Disease Control and Prevention. The progressive disease is the most common form of dementia and is associated with memory loss and cognitive decline in regions of the brain involved in thought, memory and language.

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The disease is thought to be caused by the abnormal buildup of proteins in and around the brain cells.

Today, there is no known cure for Alzheimer's, although recently approved treatments do exist that can slow the disease's progression.

"Strategies to treat Alzheimer's disease to date have largely focused on pathological changes prominent in the late stages of the disease," Scott Selleck, professor of biochemistry and molecular biology in the Penn State Eberly College of Science, said in a statement.

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"Although recently [U.S. Food and Drug Administration]-approved drugs have shown the ability to modestly slow the disease by targeting one of these changes, amyloid accumulation, drugs that affect the earliest cellular deficits might provide important tools to stop or reverse the disease process.

"We are interested in understanding the earliest cellular changes that are found not only in Alzheimer's, but shared across other neurodegenerative diseases, including Parkinson's and amyotrophic lateral sclerosis (ALS)."

In a new study published in the journal iScience, Selleck and colleagues from Penn State have identified a key molecule during these early stages of disease progression that may act as a potential target for future Alzheimer's treatments.

The discovery centers around a group of cell-signaling molecules called heparan sulfate-modified proteins, which have previously been implicated in the development of Alzheimer's disease. However, their exact role has remained unclear.

Heparan sulfate-modified proteins can be found both on the surface and in between animal cells. Among their many roles, they seem to play a key role in regulating a cellular recycling process called autophagy.

This process is known to be compromised in the early stages of several neurodegenerative diseases. And when autophagy isn't working properly, cells can't get rid of their dysfunctional or damaged components as easily, reducing their ability to repair themselves.

"In this study, we determined that heparan sulfate-modified proteins suppress autophagy-dependent cell repair," Selleck said.

The team found that disrupting the structure and function of these heparan sulfate-modified proteins increased levels of autophagy in their respective cells. What's more, reducing the function of these proteins also appeared to improve the function of the cell's mitochondria (which are responsible for energy production in the cell), and reduced the build-up of fatty compounds inside the cells—both of which are early signs of other neurodegenerative diseases.

"We demonstrate that reduced autophagy, mitochondrial defects and lipid build-up—all common changes in neurodegenerative disease—can be blocked by altering one class of proteins, those with heparan sulfate modifications," Selleck said.

"These findings suggest a promising target for future treatments that could rescue the earliest abnormalities that occur in many neurodegenerative diseases."

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