CRISPR gene-editing therapy has shown great potential to treat and even cure diseases, but scientists are now discovering how it can be used to prevent them as well. A team of researchers found a way to edit a single gene in a mosquito that prevented it from transmitting malaria, according to a paper published in Nature. These genetically modified mosquitos could eventually be released into the wild, helping prevent some of the 600,000 malaria deaths that occur each year. 

Mosquitos infect up to 263 million people yearly with malaria and efforts to reduce their populations have stalled as late. That's because both the mosquitos and their parasites that spread malaria have developed resistance to insecticides and other drugs. 

Now, biologists from UC San Diego, Johns Hopkins and UC Berkeley universities have figured out a way to stop malarial transmission by changing a single amino acid in mosquitos. The altered mosquitos can still bite people with malaria and pick up parasites from their blood, but those can no longer be spread to others. 

The system uses CRISPR-Cas9 "scissors" to cut out an unwanted amino acid (allele) that transmits malaria and replace it with a benign version. The undesirable allele, called L224, helps parasites swim to a mosquito's salivary glands where they can then infect a person. The new amino acid, Q224, blocks two separate parasites from making it to the salivary glands, preventing infection in people or animals. 

"With a single, precise tweak, we’ve turned [a mosquito gene component] into a powerful shield that blocks multiple malaria parasite species and likely across diverse mosquito species and populations, paving the way for adaptable, real-world strategies to control this disease," said researcher George Dimopoulos from Johns Hopkins University. 

Unlike previous methods of malarial control, changing that key gene doesn't affect the health or reproduction capabilities of mosquitos. That allowed the researchers to create a technique for mosquito offspring to inherit the Q224 allele and spread it through their populations to stop malarial parasite transmission in its tracks. "We’ve harnessed nature’s own genetic tools to turn mosquitoes into allies against malaria," Dimopoulos said. 

This article originally appeared on Engadget at https://www.engadget.com/science/crispr-can-stop-malaria-spread-by-editing-a-single-gene-in-mosquitos-133010031.html?src=rss

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The New York Times ran a lengthy interview this morning between columnist Ross Douthat and venture capitalist and PayPal founder Peter Thiel. There's a reason it was published in the opinion section.

Thiel, a Trump booster whose allies — including Vice President JD Vance — now litter the White House, was given free reign to discuss a variety of topics across over an hour of softball questions. Is Greta Thunberg the literal antichrist? Are the three predominant ideological schools in Europe environmentalism, "Islamic Shariah law" and "Chinese Communist totalitarian takeover"? Is AI "woke" and capable of following Elon Musk to Mars? Peter seems to think so! Perhaps the "just asking questions" school of journalism could add "hey, what the fuck are you talking about" to its repertoire. 

Admittedly, many of these assertions fall squarely into the realm of things that exist within Thiel's mind palace rather than verifiable facts, with at least one notable exception. Relatively early in their chat, Peter tells Ross the following [emphasis ours]:

If we look at biotech, something like dementia, Alzheimer’s — we’ve made zero progress in 40 to 50 years. People are completely stuck on beta amyloids. It’s obviously not working. It’s just some kind of a stupid racket where the people are just reinforcing themselves.

It's a pretty bold claim! It's also completely untrue.

"There was no treatment 40 or 50 years ago for Alzheimer's disease," Sterling Johnson, a professor of Geriatrics and Gerontology at the University of Wisconsin, Madison, told Engadget. "What we've been able to do in the last 20 years has been actually pretty extraordinary. We've developed markers that help us identify when this disease starts, using the using amyloid markers and tau biomarkers, we know that the disease actually begins 20 years before the symptoms do, and that is a critical thing to know if we are going to prevent this disease."

At the moment, Alzheimer's remains incurable. But the absence of a miracle cure does not negate the accomplishments thus far in detection and prevention. "The first treatments were these window dressing treatments. It's like treating the symptoms like you would treat a cold [...] The first generation of amyloid therapy was that kind of approach where it just addressed the symptoms by amping up the neurons and increasing the neurotransmitters available to the to the brain cells." Johnson, whose team runs one of the largest and longest studies on people at risk for developing Alzheimer's disease, added, "Now we have opportunities to actually modify the disease biology through the amyloid pathway, but also we're focused on the other proteinopathy — which is tau — and there's clinical trials underway."

Thiel, a well-known advocate for advancements in radical life extension (including a reported interest in injecting himself with the blood of young people) sees the state of scientific research in this area as sluggish and risk averse. But the groundbreaking work is happening at this moment. Professor Johnson pointed to a monoclonal antibody called gantenerumab. In an early test of 73 participants with inherited mutations that would cause them to overproduce amyloid in the brain, it cut the number of participants who developed Alzheimer's symptoms practically in half. "The big phase-three prevention trials are happening right now." Those are using lecanemab and donanemab, two other monoclonal treatments, which Johnson clarified are "already known to be better than gantenerumab at clearing out beta-amyloid."

For someone who fashions himself as a heterodox thinker, Thiel certainly seems to have stumbled on a remarkably similar talking point to current Trump administration FDA head Robert F Kennedy Jr. "Alzheimer's is a very, very good example of how [National Institute of Health] has gone off the rails over the past 20 years ago with research on amyloid plaques" Kennedy said at a Department of Health budgetary hearing last month. He claimed the NIH was "cutting off any other hypothesis" due to "corruption."

Unsurprisingly, the Alzheimer's Association has called this "demonstrably false."

"In reality, over the most recent 10 years available (2014-2023), less than 14% of new National Institutes of Health (NIH) Alzheimer’s projects focused on amyloid beta as the therapeutic target," the organization wrote, "As of September 2024, the National Institute on Aging was investing in 495 pharmacological and non-pharmacological trials. To state that Alzheimer’s research is focused on amyloid to the exclusion of other targets is clearly wrong." 

If I, personally, wanted more robust medical research and a chance at eternal life (I don't), greasing the wheels of an administration broadly gutting funding for science would be a strange way to make that happen. But this is the sort of incoherence we've come to expect from tech oligarchs: they say what benefits them, even if it's nonsense on its face, even if a moment's reflection reveals it to be patently false. What's embarrassing is the paper of record giving them free reign to do it.

Update June 27, 2025 2:15ET: This story now includes additional clinical trial information.

This article originally appeared on Engadget at https://www.engadget.com/science/peter-thiel-is-utterly-wrong-about-alzheimers-173206349.html?src=rss

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