New research on the role of a notorious Alzheimer's gene variant could pave the way to treatments that slow down or halt the disease.
Scientists found that the mutant gene, ApoE4, is directly linked to brain damage caused by knots of protein within neurons called tau tangles.
They believe targeting the gene could theoretically prevent the neurological destruction caused by Alzheimer's, for which there is currently no cure.
Lead researcher Professor David Holtzman, from Washington University School of Medicine in the US, said: "Once tau accumulates, the brain degenerates.
"What we found was that when ApoE is there, it amplifies the toxic function of tau, which means that if we can reduce ApoE levels we may be able to stop the disease process."
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ApoE4 was identified as a major risk factor for Alzheimer's disease 25 years ago.
It increases a person's risk of developing the condition by as much as 12 times.
But precisely why the gene variant is so hazardous has not been clear until now.
The scientists set out to investigate the role of ApoE, which comes in a range of different forms, or variants, in mice whose brains contained potentially toxic human tau protein.
Most experimental Alzheimer's treatments have focused on another brain symptom of the disease, clumps of beta-amyloid protein.
None of these has proved successful, the scientists pointed out.
Prof Holtzman said: "Assuming that our findings are replicated by others, I think that reducing ApoE in the brain in people who are in the earliest stages of disease could prevent further neurodegeneration."
