UF neuroscientists have confirmed a potential solution to curb the progression of Alzheimer’s disease, a neurodegenerative disorder that currently affects more than five million Americans.

A UF team specializing in neurodegenerative diseases at the William L. McKnight Brain Institute published its research Friday in the Journal of Experimental Medicine and said the work will hopefully spur the development of a new Alzheimer’s medication.

Medications on the market treat the symptoms of Alzheimer’s, but do not target the disease itself, according to a UF News release.

All neurodegenerative diseases are caused when a protein in the brain begins to fold improperly and accumulate, said Yona Levites, an assistant professor in the department of neuroscience. In the case of Alzheimer’s, the protein is called Abeta 42.

The lab conducted experiments on fruit flies and mice to study how to reduce the accumulation of Abeta 42, a protein linked to triggering Alzheimer’s, according to the release. Scientists in the lab figured out how to modulate an enzyme that makes Abeta 42 to increase the production of shorter proteins, which were once thought to be harmful, Levites said. Experiments suggest shorter proteins can protect the brain from Abeta 42 accumulation.

“This research convinces us shorter will be better,” Levites said.

The lab hopes its findings will encourage the pharmaceutical industry to develop Alzheimer’s medication using new enzyme modulators, according to the release.

Drugs using enzyme modulators are not yet safe or affordable enough to prevent Alzheimer’s later in life, Levites said. Clinical trials have failed in the past, but UF’s research can lead to Alzheimer’s immunization in the future, she said.

“Our idea is to make antibodies that will recognize Abeta 42, target it, then the body’s immune system will attack it and take it apart,” she said.

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