American scientists have identified a gene error which causes faults in the brain's nerve and blood supply system in Alzheimer's disease.
The research is promising, experts say
The gene plays a major role in determining how the systems operate, Nature Medicine reports.
But University of Rochester researchers found that expression of the gene is low in the brain cells of people with Alzheimer's disease.
Experts in the field said the research offered a promising line of study.
The scientists studied endothelial cells from the lining of blood vessels in the brain, taken from autopsy samples from people with Alzheimer's.
They found that expression of MEOX2, or mesenchyme homeobox 2, also known as GAX, was low in the cells of those with Alzheimer's.
When there are low levels of MEOX2 expression, the affected cells cannot form any form of blood supply system, and so die.
It also increased the level of a protein that removes amyloid beta peptide, the toxin that builds up in brain tissue in Alzheimer's disease.
Restoration of the gene expression level in the human brain cells was found to stimulate the formation of new blood vessels.
In further studies, one copy of the gene was deleted in mice, creating damage similar to that seen in the brains of people with Alzheimer's.
Berislav Zlokovic, who led the study, said: "This gene could be a therapeutic target. If we can stop this cycle, we could slow or stop the progression of the neuronal component of this disease.
"If we can restore the dysfunctional gene, we might be able to slow or stop the disease wherever it started."
Professor Raj Kalaria, of the Alzheimer's Research Trust, said: "This study reports a highly interesting advancement in research into Alzheimer's disease.
"This research emphasises the importance of improving the brain microcirculation in old age and possibly encouraging clearance of toxic compounds from the brain.
"The concept is akin to use of 'mental Viagra' to increase blood flow to the brain."
He added: "The discovery suggests that Alzheimer's patients are unable to form new blood vessels to possibly increase and meet the changing needs of the microcirculation in the brain.
"The report also importantly suggests that the gene may have an effect which causes a protein called amyloid to accumulate in the brains of Alzheimer's patients.
"If this is the case, this research could lead to ways to stop this protein clogging up the brain of Alzheimer's patients."
But he said the research had to be repeated to ensure it was not just a chance finding.
Susan Sorensen, head of research at the Alzheimer's Society, said: "This study seems to have identified a new target for intervention through a line of investigation not reported before."