Alzheimer’s gene neutralised in human brain cells for first time
Development comes after scientists switch away from testing on mouse cells
Scientists have claimed a major breakthrough in the battle against Alzheimer’s by neutralising a key gene that significantly increases the risk of developing the disease.
A team at Gladstone Institutes, in California, “successfully identified the protein associated with the high-risk apoE4 gene and then managed to prevent it damaging human neuron cells”, reports The Daily Telegraph.
The research, published in the journal Nature, reveals how the apoE4 gene confers its risk for Alzheimer’s in human brain cells.
“What’s more, they were able to erase the damage caused by apoE4 by changing it, with a small molecule, into a harmless apoE3-like version”, says news website ScienceDaily.
Having one copy of the apoE4 gene “more than doubles a person’s likelihood of developing Alzheimer’s disease, whereas having two copies increases the risk 12-fold”, says the Telegraph.
Previous studies “have indicated that roughly one in four people carry the gene”, the newspaper reports.
The latest breakthrough adds to hopes of finding a drug treatment that could halt the onset of the disease. The researchers have urged caution, however, pointing out that the neutralising process has only been tried in lab conditions as yet.
The development came after the California team decided to shun traditional testing methods.
Most Alzheimer’s research and drug development “are done in mouse models of the disease”, says ScienceDaily.
“Drug development for Alzheimer's disease has been largely a disappointment over the past ten years,” says lead study author Yadong Huang. “Many drugs work beautifully in a mouse model, but so far they’ve all failed in clinical trials. One concern within the field has been how poorly these mouse models really mimic human disease.”
Following a succession of clinical trial failures, Huang and his colleagues decided to use human cells to model the disease and test new drugs, leading to their discovery.