University of Chicago researchers engaged in preclinical research have redeemed amyloid precursor protein (APP), a contributor to Alzheimer’s disease, as an unlikely hero by uncovering its expanded role in brain signaling that can prevent the development of Alzheimer’s disease in mice reports Xinhuanet.
The researchers posted the study on the University of Chicago website this past week.
The University of Chicago preclinical investigators fashioned a sticky lipid anchor protein from natural APP, and injected this modified APP segment, called the mAIC, into mice.
Genetically-engineered to be afflicted with aggressive Alzheimer’s disease at a young age, the mice would have normally suffered from the advanced symptoms of the disease as young as six months old—equivalent to a young adult in humans.
After the injection, the team tested the mice’s ability to form spatiotemporal memories. Equipped with a general helping of mAICD, these mice successfully recalled or ignored objects and places previously explored. But on the other hand, the control mice with Alzheimer’s who expressed a less interactive version of mAICD, did not recognize supposedly familiar objects and locations at all.
They were already gripped by the jaws of the disease. A researcher noted that the mice with mAICD became almost normal—it was as if they never had signs of Alzheimer’s disease. The lipid anchor protein was able to keep Alzheimer’s disease at bay in these mice, as long as its expression starts during the brain development stage.
Researchers are now aware that APP can stimulate the growth of new neurons and strengthen synaptic activity by triggering a series of events associated with memory consolidation.
The University of Chicago team continues the investigation focusing on the effects of the same mAICD intervention in the brains of adult mice already afflicted with Alzheimer’s.
Angele Parent, associate professor of neurobiology