Six months after researchers in China bioengineered monkeys to have autism, a Japanese team of scientists has used the same technology to create monkeys with Parkinson’s. It’s a scientific first, and it could lead to effective treatments—but do the ends justify the means?
As reported in New Scientist, a team led by Hideyuki Okano from the Keio University School of Medicine in Tokyo has used genetic engineering to create a marmoset monkey with Parkinson’s disease. The researchers unveiled the monkeys last month at a meeting in Alpbach, Austria, and say they’ve also bioengineered monkeys to mimic Alzheimer’s disease and motor neurone disease. These monkeys are now three years old, and they’ve already started to exhibit the tell-tale signs of Parkinson’s.
As fellow primates, monkeys are ideal candidates for this type of medical research. As noted, scientists in China have already built autistic monkeys, and thanks to the CRISPR gene-editing tool, there are plans to create monkeys with an assortment of other human-specific diseases, including schizophrenia and severe immune dysfunction.
These animals are increasingly being seen as viable research subjects because humans and monkeys share similar brains and bodies. At the same time, medical experiments on great apes are being phased out, while research on mice is limited in scope. Also, the lack of public support for primate research in North America and Europe is not shared in Asia. As it stands, there are currently 40 breeding companies working in China which have collectively produced nearly 300,000 monkeys, all of which could be used for scientific research.
To create the Parkinson’s monkeys, Okano’s team isolated a mutated version of a human gene called SNCA, which is linked to the disorder. Writing in New Scientist, Andy Coghlan explains what this modified gene is doing to the marmosets:
In the three years since the engineered marmosets were born, they developed Parkinson’s symptoms in the same way people do. This began with signs of sleep disturbance in their first year, followed by the appearance of a-synuclein-associated globules, known as Lewy bodies, in their brain stems the next year.
By their third year, the monkeys began to show the characteristic tremors associated with the condition. As further evidence of how similar these monkeys are to humans with Parkinson’s, Okano showed that their tremors could be eased by giving them L-DOPA, a drug given to people with Parkinson’s to make up for the lack of dopamine.
Some scientists are excited about the opportunity to study Parkinson’s in a nonhuman model, but critics say there’s no guarantee these results will translate to humans. It’s also worth pointing out that most human diseases aren’t caused by a single faulty gene, so these monkeys will likely be of limited clinical relevance.
Finally, there’s the ethics of it all. Given the severity of Parkinson’s symptoms, this type of animal experimentation is both cruel and unusual. As Princeton bioethicist Peter Singer has said, “Animals are an end unto themselves because their suffering matters.”