A study conducted by UF researchers may be a beginning step in developing a drug to slow the progression of Alzheimer’s disease.
For about five years, researchers have been conducting this study using genetically engineered mice. David Borchelt, a UF professor of neuroscience, said the mice don’t have the complete type of Alzheimer’s that is seen in humans, but they have the early pathology changes.
“They produce a particular kind of brain lesion that’s called amyloid plaque,” he said. “They’re the same kind of plaques that we find in people with Alzheimer’s disease.”
After the plaques form, people with Alzheimer’s develop another brain pathology called a neurofibrillary tangle, which are structures that form inside the brain cells.
“They seem to be the structures that lead to the most profound dysfunction of those cells and eventually will kill them,” Borchelt said.
Researchers were using the mice to analyze whether there were changes in brain cell function as a result of the plaque. They were looking for how the tangle eventually shows up in humans with Alzheimer’s, Borchelt said.
He said they found that accumulation of the amyloid pathology does cause general problems in protein metabolism in the mice. These findings give a new kind of symptom in mice that can now be utilized to look for drugs that would correct it.
The idea is if researchers can correct that symptom in mice and slow the transition from the amyloid plaque to the tangle, then they might be able to slow down progression of the human disease, Borchelt said.
Guilian Xu, an assistant research scientist at the UF College of Medicine, said there is no direct benefit for Alzheimer’s patients at this point.
“If we find the exact difference between mouse and human, then somebody can develop a drug to target that critical step,” she said.
