Treatment From Brain Tissue May Have Spread Alzheimer's Protein
It may be possible to transmit Alzheimer's disease from one person to another, according to a study published Wednesday in Nature. But this would occur only in highly unusual circumstances involving direct exposure to brain tissue, scientists say.
"This relates to a very special situation where people have been injected with, essentially, extracts of human [brain] tissue," said John Collinge, head of the Department of Neurodegenerative Disease at University College London, during a press conference about the study. "You can't catch Alzheimer's disease by taking care of someone with Alzheimer's disease."
The study involved autopsies of eight people who had received injections of human growth hormone as children more than 30 years ago. The growth hormone, extracted from human pituitary glands, had been tainted with a protein that caused these people to develop a fatal brain disease called Creutzfeldt-Jakob disease.
Researchers performed the autopsies to see if there was anything else unusual about the brains of these individuals. "And what we found, very much to our surprise, is that four of them had really quite significant deposition of Alzheimer amyloid protein in their brains," Collinge said.
Amyloid protein is what forms the sticky plaques that appear in the brains of people with Alzheimer's. But the individuals in the study had died far too young (the oldest was just 51) to have so much amyloid in their brains.
So the researchers began searching for an explanation. And they concluded that the growth hormone had been tainted with a second protein from the human pituitary glands — one that caused amyloid to build up quickly.
There's no way this could happen now, because growth hormone hasn't been made from brain tissue since the 1980s. Also, the people in the study did not have full-blown Alzheimer's, only the amyloid deposits that typically appear before problems with memory and thinking.
But the finding could have implications for surgeons operating on the brains of people with Alzheimer's, says Lary Walker, a neuroscientist at Emory University and the Yerkes National Primate Research Center.
"It's possible that contaminated surgical instruments might be able to transfer seeds to another patient in the next surgery," Walker says, adding that this is a remote possibility.
The importance of the autopsy study is its finding that Alzheimer's has a lot in common with so-called prion diseases. They include Creutzfeldt-Jakob in people, the very similar mad cow disease in cattle, and scrapie in sheep and goats, Walker says. Prion diseases and Alzheimer's both appear to involve rogue proteins that fold into abnormal shapes and then form toxic clusters or seeds, he says.
The new study "reinforces what many in the field have been thinking for a while, and that is that we need to prevent the accumulation of these proteins in the brain if we are to do anything substantive about Alzheimer's disease," Walker says.
Research on prion diseases in animals shows that drugs can help clear away the misfolded proteins that allow these diseases to progress, says Bill Rebeck, a neuroscientist at Georgetown University. And the new study raises the possibility that similar drugs might keep Alzheimer's from getting worse in patients whose brains are already damaged.
"I think what this speaks about is the exciting idea that maybe we can prevent [Alzheimer's] from spreading from one region to another, thus halting the inevitable progression of symptoms," he says.
Several human brain diseases appear to involve misfolded protein seeds that cause damage to spread throughout the brain, Rebeck says. So an approach that worked in one of these diseases might well work for all of them.
"The idea that we could be promoting processes that clear away any misfolded protein, in theory that would be useful against prion diseases, or Parkinson's disease or Alzheimer's disease or Huntington's disease," Rebeck says.
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