University of California-San Francisco researchers said the mouse model, which expresses the same mutant proteins as human Parkinson's patients, also displays early signs of constipation and other gastrointestinal problems that are a common harbinger of the disease in humans.
The scientists, led by Dr. Robert Nussbaum, said that means the animals could serve as a way of investigating therapies for reversing the neurological dysfunction of the disease at its earliest stages.
The gastrointestinal dysfunction could be seen at three months of age, reached its highest severity at six months and persisted until 18 months, which the scientists said follows the human course of the disease in sporadic Parkinson's disease. That dysfunction occurred before there was any evidence of loss of smell or pathological changes in the brain stem.
"This suggests that, at least in mice with the human proteins, these gastrointestinal symptoms are an intrinsic defect caused by the mutant protein, rather than being caused by abnormalities in brain function," Yien-Ming Kuo, the study's lead author, said. "That knowledge could eventually help us test for the disease long before it starts to cause neurodegenerative problems and prevent them from occurring."
The study appears in the journal Human Molecular Genetics.