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Can you catch Alzheimer's?
NEWS & TECHNOLOGY
Can you catch Alzheimer’s? A rogue protein may spread Alzheimer’s disease via blood transfusions This suggests Alzheimer’s can shared a blood system. indeed spread via beta-amyloid The healthy mice started to in blood. “The protein can get into accumulate beta-amyloid in their the brain from a connected mouse brains. Within four months, the and cause neurodegeneration,” mice also had altered patterns of says Weihong Song at the activity in brain regions that are University of British Columbia key for learning and memory in Canada, who led the work. (Molecular Psychiatry, doi.org/ Song’s team carried out the cfqh). It is the first time that betastudy on mice with a gene that “It strengthens the case makes the human version of that beta-amyloid is beta-amyloid, because the infectious. It may actually animals don’t normally develop be a prion or like one” Alzheimer’s. This gene meant the mice developed brain plaques and neurodegeneration. amyloid has been found to enter The team then surgically the blood and brain of another attached mice with this mouse and cause signs of Alzheimer’s-like condition to Alzheimer’s disease, says Song. healthy mice without the beta“They somewhat convincingly amyloid gene, so that they show that it is possible to induce
FEAR has been growing that Alzheimer’s disease might be capable of spreading via blood transfusions, but it has been hard to find any evidence that this is happening. Now a study has found that an Alzheimer’s protein can pass between mice sharing a blood supply. We know from prion diseases like Creutzfeldt-Jakob Disease (CJD) that misfolded proteins can spread brain conditions. Variant CJD, for example, can spread via meat products or blood transfusions infected with prions. Alzheimer’s also involves a misfolded protein, called betaamyloid. Plaques of this protein accumulate in the brains of people with the condition, although we still don’t know if the plaques cause Alzheimer’s, or are merely a symptom. There’s some evidence that beta-amyloid may spread like prions. Around 50 years ago, people with a growth disorder were treated with growth hormone taken from cadavers. Many of the recipients went on to develop CJD, because the tissue from these cadavers turned out to be carrying prions. Decades later, it emerged in postmortems that some of these people also had Alzheimer’s plaques, despite being relatively young. The team behind this work raised the possibility that some medical or surgical procedures may pose a risk. Now a study has found that, when a healthy mouse is conjoined with a mouse that has Alzheimer’s plaques, it will start to develop plaques of betaamyloid protein in its own brain. When the plaques form, their brain tissue starts to die. 6 | NewScientist | 4 November 2017
ZEPHYR/SCIENCE PHOTO LIBRARY
Jessica Hamzelou
[plaques] in mice just by connecting the circulation,” says Gustaf Edgren at the Karolinska Institute in Stockholm, Sweden. “It strengthens the case that betaamyloid is infectious somehow – it may actually be a prion or act like a prion.” These findings contradict a study earlier this year by Edgren and his colleagues, which tracked 2.1 million recipients of blood transfusions across Sweden and Denmark. They found that those who received blood from people with Alzheimer’s didn’t seem to be at any greater risk of developing the disease. Edgren says that there’s a chance his study didn’t run for long enough to catch evidence that Alzheimer’s proteins might be transmissible. “It could take a long time [for the disease to develop], or there could not be enough data. A lot of researchers fear that it’s an infectious protein,” he says. Song’s team says it is too soon to draw conclusions. Stitching mice together is not a situation that applies to people, says Edgren. Mathias Jucker at the German Center for Neurodegenerative Diseases in Tübingen doesn’t think the study shows that Alzheimer’s is a transmissible disease. And the team has not yet looked at the behaviour of the mice to see if they show signs of the cognitive decline characteristic of Alzheimer’s. One of the reasons it has been hard to treat Alzheimer’s is the difficulty of designing drugs that can cross the brain’s protective barrier. So the findings may lead to new medical approaches. It may be easier to target the protein in the bloodstream, which could have knock-on effects for the –Shrunken: a brain on Alzheimer’s– brain, says Song. n
Can you catch Alzheimer’s? A rogue protein may spread Alzheimer’s disease via blood transfusions This suggests Alzheimer’s can shared a blood system. indeed spread via beta-amyloid The healthy mice started to in blood. “The protein can get into accumulate beta-amyloid in their the brain from a connected mouse brains. Within four months, the and cause neurodegeneration,” mice also had altered patterns of says Weihong Song at the activity in brain regions that are University of British Columbia key for learning and memory in Canada, who led the work. (Molecular Psychiatry, doi.org/ Song’s team carried out the cfqh). It is the first time that betastudy on mice with a gene that “It strengthens the case makes the human version of that beta-amyloid is beta-amyloid, because the infectious. It may actually animals don’t normally develop be a prion or like one” Alzheimer’s. This gene meant the mice developed brain plaques and neurodegeneration. amyloid has been found to enter The team then surgically the blood and brain of another attached mice with this mouse and cause signs of Alzheimer’s-like condition to Alzheimer’s disease, says Song. healthy mice without the beta“They somewhat convincingly amyloid gene, so that they show that it is possible to induce
FEAR has been growing that Alzheimer’s disease might be capable of spreading via blood transfusions, but it has been hard to find any evidence that this is happening. Now a study has found that an Alzheimer’s protein can pass between mice sharing a blood supply. We know from prion diseases like Creutzfeldt-Jakob Disease (CJD) that misfolded proteins can spread brain conditions. Variant CJD, for example, can spread via meat products or blood transfusions infected with prions. Alzheimer’s also involves a misfolded protein, called betaamyloid. Plaques of this protein accumulate in the brains of people with the condition, although we still don’t know if the plaques cause Alzheimer’s, or are merely a symptom. There’s some evidence that beta-amyloid may spread like prions. Around 50 years ago, people with a growth disorder were treated with growth hormone taken from cadavers. Many of the recipients went on to develop CJD, because the tissue from these cadavers turned out to be carrying prions. Decades later, it emerged in postmortems that some of these people also had Alzheimer’s plaques, despite being relatively young. The team behind this work raised the possibility that some medical or surgical procedures may pose a risk. Now a study has found that, when a healthy mouse is conjoined with a mouse that has Alzheimer’s plaques, it will start to develop plaques of betaamyloid protein in its own brain. When the plaques form, their brain tissue starts to die. 6 | NewScientist | 4 November 2017
ZEPHYR/SCIENCE PHOTO LIBRARY
Jessica Hamzelou
[plaques] in mice just by connecting the circulation,” says Gustaf Edgren at the Karolinska Institute in Stockholm, Sweden. “It strengthens the case that betaamyloid is infectious somehow – it may actually be a prion or act like a prion.” These findings contradict a study earlier this year by Edgren and his colleagues, which tracked 2.1 million recipients of blood transfusions across Sweden and Denmark. They found that those who received blood from people with Alzheimer’s didn’t seem to be at any greater risk of developing the disease. Edgren says that there’s a chance his study didn’t run for long enough to catch evidence that Alzheimer’s proteins might be transmissible. “It could take a long time [for the disease to develop], or there could not be enough data. A lot of researchers fear that it’s an infectious protein,” he says. Song’s team says it is too soon to draw conclusions. Stitching mice together is not a situation that applies to people, says Edgren. Mathias Jucker at the German Center for Neurodegenerative Diseases in Tübingen doesn’t think the study shows that Alzheimer’s is a transmissible disease. And the team has not yet looked at the behaviour of the mice to see if they show signs of the cognitive decline characteristic of Alzheimer’s. One of the reasons it has been hard to treat Alzheimer’s is the difficulty of designing drugs that can cross the brain’s protective barrier. So the findings may lead to new medical approaches. It may be easier to target the protein in the bloodstream, which could have knock-on effects for the –Shrunken: a brain on Alzheimer’s– brain, says Song. n