Scientists have identified two proteins that may help prevent the brain plaques that are linked to Alzheimer's disease.
Alzheimer's causes damage to the brain
The proteins appear to work in tandem to orchestrate removal of potentially hazardous molecules from the brain.
However, unless the two are in the correct balance they actually seem to promote deposition of the amyloid protein which forms the plaques.
The research, by Washington University of Medicine, St Louis, is published in the journal Neuron.
The key proteins are called apoliprotein E (apoE) and clusterin.
Lead researcher Professor David Holtzman said: "This is one of the first demonstrations in living animals that these proteins affect amyloid clearance.
"Our findings suggest it is worthwhile to explore the use of drugs or therapies to alter or perhaps increase the expression of these proteins as a potential treatment for Alzheimer's disease."
Studies suggest that plaques form when the protein amyloid beta is converted from its soluble to its insoluble form and forms stringy threads that build into tangles.
In previous studies, Professor Holtzman's team has shown that both apoE and clusterin promote the formation of plaques.
Sure enough in their latest study mice developed fewer plaques when they were genetically engineered to lack either one of the two proteins.
However, mice that lacked both proteins - far from developing even fewer deposits - actually developed them significantly earlier in life.
Such extreme deposition at a young age is akin to that in humans with the rare, genetic form of the disease called familial Alzheimer's.
The mice who lacked apoE and clusterin showed signs of higher levels of amyloid protein not only in their brain tissue, also in the fluid surrounding individual brain cells and the fluid surrounding the entire brain.
Professor Holtzman said the result implied that apoE and clusterin worked together to suppress plaque formation by clearing amyloid protein from the brain tissue and surrounding fluid.
Without its chaperones, the amyloid protein settles in the brain and eventually clusters into plaques.
Professor Holtzman said the next step was to determine whether human forms of apoE and clusterin also delay or prevent the development of plaques.
Harriet Millward, of the UK Alzheimer's Research Trust, said: "The two proteins studied in this research probably have critical roles in Alzheimer's disease, but their functions are so complex we do not know what their roles actually are.
"We look forward to seeing the full details of this study which seems to offer valuable and interesting results, but unfortunately we are still a long way from finding an answer to Alzheimer's disease."