Knocking back an enzyme swept mouse brains clean of protein globs that are a sign of Alzheimer’s disease. Reducing the enzyme is known to keep these nerve-damaging plaques from forming. But the disappearance of existing plaques was unexpected, researchers report online February 14 in the Journal of Experimental Medicine.

The brains of mice engineered to develop Alzheimer’s disease were riddled with these plaques, clumps of amyloid-beta protein fragments, by the time the animals were 10 months old. But the brains of 10-month-old Alzheimer’s mice that had a severely reduced amount of an enzyme called BACE1 were essentially clear of new and old plaques.
Studies rarely demonstrate the removal of existing plaques, says neuroscientist John Cirrito of Washington University in St. Louis who was not involved in the study. “It suggests there is something special about BACE1,” he says, but exactly what that might be remains unclear.

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One theory to how Alzheimer’s develops is called the amyloid cascade hypothesis. Accumulation of globs of A-beta protein bits, the idea goes, drives the nerve cell loss and dementia seen in the disease, which an estimated 5.5 million Americans had in 2017. If the theory is right, then targeting the BACE1 enzyme, which cuts up another protein to make A-beta, may help patients.
BACE1 was discovered about 20 years ago. Initial studies turned off the gene that makes BACE1 in mice for their entire lives, and those animals produced almost no A-beta. In humans, however, any drug that combats Alzheimer’s by going after the enzyme would be given to adults. So Riqiang Yan, one of the discoverers of BACE1 and a neuroscientist at the Cleveland Clinic, and colleagues set out to learn what happens when mice who start life with normal amounts of BACE1 lose much of the enzyme later on.

The researchers studied mice engineered to develop plaques in their brains when the animals are about 10 weeks old. Some of these mice were also engineered so that levels of the BACE1 enzyme, which is mostly found in the brain, gradually tapered off over time. When these mice were 4 months old, the animals had lost about 80 percent of the enzyme.
Alzheimer’s mice with normal BACE1 levels experienced a steady increase in plaques, clearly seen in samples of their brains. In Alzheimer’s mice without BACE1, however, the clumps followed a different trajectory. The number of plaques initially grew, but by the time the mice were around 6 months old, those plaques had mostly disappeared. And by 10 months, “we hardly see any,” Yan says.

Cirrito was surprised that getting rid of BACE1 later in life didn’t just stop plaques from forming, but removed them, too. “It is possible that perhaps a therapeutic agent targeting BACE1 in humans might have a similar effect,” he says.

Drugs that target BACE1 are already in development. But the enzyme has other jobs in the brain, such as potentially affecting the ability of nerve cells to communicate properly. It may be necessary for a drug to inhibit some, but not all, of the enzyme, enough to prevent plaque formation but also preserve normal signaling between nerve cells, Yan says.

What a spectacular Easter basket tardigrade eggs would make — at least for those celebrating in miniature.

A new species of the pudgy, eight-legged, water creatures lays pale, spherical microscopic eggs studded with domes crowned in long, trailing streamers.

Eggs of many land-based tardigrades have bumps, spines, filaments and such, presumably to help attach to a surface, says species codiscoverer Kazuharu Arakawa. The combination of a relatively plain surface on the egg itself (no pores, for instance) plus a filament crown helps distinguish this water bear as a new species, now named Macrobiotus shonaicus, he and colleagues report February 28 in PLOS ONE.
With about 20 new species added each year to the existing 1,200 or so known worldwide, tardigrades have become tiny icons of extreme survival (SN Online: 7/14/17).

“I was actually not looking for a new species,” Arakawa says. He happened on it when searching through moss he plucked from the concrete parking lot at his apartment. He routinely samples such stray spots to search for tardigrades, one of his main interests as a genome biologist at Keio University’s Institute for Advanced Biosciences in Tsuruoka City, Japan.
These particular moss-loving creatures managed to grow and reproduce in the lab —“very rare for a tardigrade,” he says. He didn’t realize it was an unknown species until he started deciphering the DNA that makes up some of its genes. The sequences he found didn’t match any in a worldwide database.

His two coauthors, at Jagiellonian University in Krakow, Poland, worked out that he had found a new member of a storied cluster of relatives of the tardigrade M. hufelandi. That species, described in 1834, kept turning up across continents around the world — or so biologists thought for more than a century. Realization eventually dawned that the single species that could live in such varied places was actually a complex of close cousins.

And now M. shonaicus adds yet another cousin to a group of about 30. Who knows where the next one will turn up. “I think there are lots more to be identified,” Arakawa says.

Adult mice and other rodents sprout new nerve cells in memory-related parts of their brains. People, not so much. That’s the surprising conclusion of a series of experiments on human brains of various ages first described at a meeting in November (SN: 12/9/17, p. 10). A more complete description of the finding, published online March 7 in Nature, gives heft to the controversial result, as well as ammo to researchers looking for reasons to be skeptical of the findings.

In contrast to earlier prominent studies, Shawn Sorrells of the University of California, San Francisco and his colleagues failed to find newborn nerve cells in the memory-related hippocampi of adult brains. The team looked for these cells in nonliving brain samples in two ways: molecular markers that tag dividing cells and young nerve cells, and telltale shapes of newborn cells. Using these metrics, the researchers saw signs of newborn nerve cells in fetal brains and brains from the first year of life, but they became rarer in older children. And the brains of adults had none.

There is no surefire way to spot new nerve cells, particularly in live brains; each way comes with caveats. “These findings are certain to stir up controversy,” neuroscientist Jason Snyder of the University of British Columbia writes in an accompanying commentary in the same issue of Nature.

THE WOODLANDS, Texas — Venus’ crust is broken up into chunks that shuffle, jostle and rotate on a global scale, researchers reported in two talks March 20 at the Lunar and Planetary Science Conference.

New maps of the rocky planet’s surface, based on images taken in the 1990s by NASA’s Magellan spacecraft, show that Venus’ low-lying plains are surrounded by a complex network of ridges and faults. Similar features on Earth correspond to tectonic plates crunching together, sometimes creating mountain ranges, or pulling apart. Even more intriguing, the edges of the Venusian plains show signs of rubbing against each other, also suggesting these blocks of crust have moved, the researchers say.
“This is a new way of looking at the surface of Venus,” says planetary geologist Paul Byrne of North Carolina State University in Raleigh.

Geologists generally thought rocky planets could have only two forms of crust: a stagnant lid as on the moon or Mars — where the whole crust is one continuous piece — or a planet with plate tectonics as on Earth, where the surface is split into giant moving blocks that sink beneath or collide with each other. Venus was thought to have one solid lid (SN: 12/3/11, p. 26).

Instead, those options may be two ends of a spectrum. “Venus may be somewhere in between,” Byrne said. “It’s not plate tectonics, but it ain’t not plate tectonics.”

While Earth’s plates move independently like icebergs, Venus’ blocks jangle together like chaotic sea ice, said planetary scientist Richard Ghail of Imperial College London in a supporting talk.
Ghail showed similar ridges and faults around two specific regions on Venus that resemble continental interiors on Earth, such as the Tarim and Sichuan basins in China. He named the two Venusian plains the Nuwa Campus and Lada Campus. (The Latin word campus translates as a field or plain, especially one bound by a fence, so he thought it was fitting.)
Crustal motion may be possible on Venus because the surface is scorching hot (SN: 3/3/18, p. 14). “Those rocks already have to be kind of gooey” from the high temperatures, Byrne said. That means it wouldn’t take a lot of force to move them. Venus’ interior is also probably still hot, like Earth’s, so convection in the mantle could help push the blocks around.

“It’s a bit of a paradigm shift,” says planetary scientist Lori Glaze of NASA’s Goddard Space Flight Center, who was not involved in the new work. “People have always wanted Venus to be active. We believe it to be active, but being able to identify these features gives us more of a sense that it is.”

The work may have implications for astronomers trying to figure out which Earth-sized planets in other solar systems are habitable (SN: 4/30/16, p. 36). Venus is almost the same size and mass as the Earth. But no known life exists on Venus, where the average surface temperature is 462° Celsius and the atmosphere is acidic. Scientists have long speculated that the planet’s apparent lack of plate tectonics might play a role in making the planet so seemingly uninhabitable.

What’s more, the work also underlines the possibility that planets go through phases of plate tectonics (SN: 6/25/16, p. 8). Venus could have had plate tectonics like Earth 1 billion or 2 billion years ago, according to a simulation presented at the meeting by geophysicist Matthew Weller of the University of Texas at Austin.

“As Venus goes, does that predict where the Earth is going in the relatively near future?” he wondered.