An experimental treatment appears to delay Alzheimer’s symptoms in some people genetically destined to get the disease in their 40s or 50s, according to new findings from ongoing research now caught up in Trump administration funding delays.

The early results — a scientific first — were published Wednesday even as study participants worried that politics could cut their access to a possible lifeline.

“It’s still a study but it has given me an extension to my life that I never banked on having,” said Jake Heinrichs of New York City.

Now 50, Heinrichs has been treated in that study for more than a decade and remains symptom-free despite inheriting an Alzheimer’s-causing gene that killed his father and brother around the same age.

If blocked funding stops Heinrichs’ doses, “how much time do we have?” asked his wife, Rachel Chavkin. “This trial is life.”

Two drugs sold in the U.S. can modestly slow worsening of early-stage Alzheimer’s by clearing the brain of one of its hallmarks, a sticky gunk called amyloid. But until now, there haven’t been hints that removing amyloid far earlier – many years before the first symptoms appear – just might postpone the disease.

The research led by Washington University in St. Louis involves families that pass down rare gene mutations almost guaranteeing they’ll develop symptoms at the same age their affected relatives did – information that helps scientists tell if treatments are having any effect.

The new findings center on a subset of 22 participants who received amyloid-removing drugs the longest, on average eight years. Long-term amyloid removal cut in half their risk of symptom onset, researchers reported Wednesday in the journal Lancet Neurology.

Despite the study’s small size, “it’s incredibly important,” said Northwestern University neuroscientist David Gate, who wasn’t involved with the research.

Now participants have been switched from an earlier experimental drug to Leqembi, an IV treatment approved in the U.S., to try to answer the obvious next question.

“What we want to determine over the next five years is how strong is the protection,” said Washington University’s Dr. Randall Bateman, who directs the Dominantly Inherited Alzheimer’s Network of studies involving families with these rare genes. “Will they ever get the symptoms of Alzheimer’s disease if we keep treating them?”

Here’s the worry: Bateman raised money to start that confirmatory study while seeking National Institutes of Health funding for the full project but his grant has been delayed as required reviews were canceled. It’s one example of how millions of dollars in research have been stalled as NIH grapples with funding restrictions and mass firings.

At the same time researchers wonder if NIH will shift focus away from amyloid research after comments by Dr. Jay Bhattacharya, nominated as the agency’s new director.

“One of the reasons I think that we have not made progress in Alzheimer’s, as much as we ought to have, is because the NIH has not supported a sufficiently wide range of hypotheses,” Bhattacharya told senators, responding to one who brought up an example of earlier science misconduct unrelated to current research.

Scientists don’t know exactly what causes Alzheimer’s, a mind-destroying disease that affects nearly 7 million Americans, mostly late in life. What’s clear is that silent changes occur in the brain at least two decades before the first symptoms — and that sticky amyloid is a major contributor. At some point amyloid buildup appears to trigger a protein named tau to begin killing neurons, which drives cognitive decline.

Tau-fighting drugs now are being tested. Researchers also are studying other factors including inflammation, the brain’s immune cells and certain viruses.

NIH’s focus expanded as researchers found more potential culprits. In 2013, NIH’s National Institute on Aging funded 14 trials of possible Alzheimer’s drugs, over a third targeting amyloid. By last fall, there were 68 drug trials and about 18% targeted amyloid.

Northwestern’s Gate counts himself among scientists who “think amyloid isn’t everything,” but said nothing has invalidated the amyloid hypothesis. He recently used brain tissue preserved from an old amyloid study to learn how immune cells called microglia can clear those plaques and then switch to helping the brain heal, possible clues for improving today’s modest therapies.

For now, amyloid clearly is implicated somehow and families with Alzheimer’s-causing genes are helping answer a critical question for anyone at risk: Can blocking amyloid buildup really stave off symptoms? Without NIH funding, Bateman said, that opportunity will be lost.

“It’s absolutely insane,” said longtime study participant June Ward, who lives near Asheville, North Carolina, and plans to ask friends to complain to lawmakers.

Ward turns 64 in June and is healthy, two years older than when her mother’s symptoms appeared. “It is exciting to think about the possibility that Alzheimer’s disease might not be what gets me,” she said.

In New York, Heinrichs said he has hope that his 3-year-old son won’t “experience the stress and sorrow that I lived through as a young man to watch my father fade away.”

“We need the NIH to be not politicized,” added Chavkin, his wife. “It’s just about keeping people alive or helping them live better. And in this case, it’s helping my husband survive.”

—-

The Associated Press Health and Science Department receives support from the Howard Hughes Medical Institute’s Science and Educational Media Group and the Robert Wood Johnson Foundation. The AP is solely responsible for all content.

SANTA FE, N.M. — SANTA FE, N.M. (AP) — Actor Gene Hackman died of heart disease a full week after his wife died from hantavirus in their New Mexico hillside home, likely unaware that she was dead because he was in the advanced stages of Alzheimer’s disease, authorities revealed Friday.

Both deaths were ruled to be from natural causes, chief medical examiner Dr. Heather Jarrell said alongside state fire and health officials at a news conference.

“Mr. Hackman showed evidence of advanced Alzheimer’s disease,” Jarrell said. “He was in a very poor state of health. He had significant heart disease, and I think ultimately that’s what resulted in his death.”

Authorities didn’t suspect foul play after the bodies of Hackman, 95, and Betsy Arakawa, 65, were discovered Feb 26. Immediate tests for carbon monoxide poisoning were negative.

Investigators found that the last known communication and activity from Arakawa was Feb. 11 when she visited a pharmacy, pet store and grocery before returning to their gated neighborhood that afternoon, Santa Fe County Sheriff Adan Mendoza said Friday.

Hackman’s pacemaker last showed signs of activity a week later and that he had an abnormal heart rhythm Feb. 18, the day he likely died, Jarrell said.

Although there was no reliable way to determine the date and time when both died, all signs point to their deaths coming a week apart, Jarrell said.

“It’s quite possible he was not aware she was deceased,” Jarrell said.

Dr. Michael Baden, a former New York City medical examiner, said he believes Hackman was severely impaired due to Alzheimer’s disease and unable to deal with his wife’s death in the last week of his life.

Most older Americans with dementia live at home, and many receive care from family or friends.

Their bodies were found a little over a week later. Hackman was found in the home’s entryway. His death was tied to heart disease with Alzheimer’s disease contributing.

Arakawa was found in a bathroom. Authorities linked her death to hantavirus pulmonary syndrome, a rare but potentially fatal disease spread by infected rodent droppings. Thyroid medication pills prescribed to Arakawa were found nearby and weren’t listed as contributing to her death, Jarrell said.

Hantavirus typically is reported in spring and summer, often due to exposures that occur when people are near mouse droppings in homes, sheds or poorly ventilated areas. This is the first confirmed case of hantavirus in New Mexico this year.

While hantavirus is found throughout the world, most cases in the U.S. have been found in western states. The virus can cause a severe and sometimes deadly lung infection.

Jarrell said it was not known how quickly Arakawa died.

One of the couple’s three dogs also was found dead in a crate in a bathroom closet near Arakawa, while two other dogs survived. Authorities initially misidentified the breed.

Dogs do not get sick from hantavirus, said Erin Phipps, a veterinarian with the New Mexico Health Department. The sheriff considers this an open investigation until they receive results of the dog’s necropsy and finish checking into data from personal cellphones retrieved from the home.

When Hackman and Arakawa were found, the bodies were decomposing with some mummification, a consequence of body type and climate in Santa Fe’s especially dry air at an elevation of nearly 7,200 feet (2,200 meters).

“All of us that knew him should have been checking on him,” said Stuart Ashman, co-owner of Artes de Cuba gallery who cherished his encounters with Hackman at a local Pilates exercise studio, where they used to swap stories. “I had no idea. … It’s just really sad. And that she died a week before him. My God.”

Dr. Victor Weedn, a forensic pathologist in Virginia, said when two bodies are found at the same time, the usual assumption would be that they died at the same time. But Hackman’s Alzheimer’s disease added a complicating factor: He apparently was unable to seek help after his wife died.

“They died several days apart: One dying of a viral infection, the hantavirus, which can kill quite quickly. And the other death occurring from heart disease. And that too can be a relatively sudden death,” Weedn said. “Their (the authorities’) explanation, I thought, was quite clear and plausible. I believe they really discovered what truly happened in this case.”

Hackman, a Hollywood icon, won two Oscars during a storied career in films including “The French Connection,” “Hoosiers” and “Superman” from the 1960s until his retirement in the early 2000s.

Arakawa, born in Hawaii, studied as a concert pianist, attended the University of Southern California and met Hackman in the mid-1980s while working at a California gym.

Hackman dedicated much of his time in retirement to painting and writing novels far from Hollywood’s social circuit. He served for several years on the board of trustees at the Georgia O’Keeffe Museum in Santa Fe, and he and his wife were investors in local businesses.

___

Baumann reported from Bellingham, Washington. Associated Press reporters Jacques Billeaud in Phoenix, John Seewer in Toledo, Ohio, and Carla Johnson in Seattle contributed.

A European regulatory committee now recommends approval of the Alzheimer’s treatment lecanemab a few months after rejecting the drug.

Biogen said Thursday that the drug, known in the U.S. as Leqembi, received a positive opinion from the European Medicines Agency’s Committee for Medicinal Products for Human Use as a treatment for early Alzheimer’s disease.

The European Commission is now expected to make a marketing authorization decision in the next few months.

The committee had said in July that concerns about the drug’s potential side effects outweigh the impact it has in slowing the fatal, mind-robbing disease. But Japanese drugmaker Eisai asked the committee to reconsider its decision.

Eisai developed Leqembi and is co-marketing it with Cambridge, Massachusetts-based Biogen Inc.

Leqembi clears a sticky brain plaque linked to the disease. A large study has shown that it slowed memory and thinking decline by several months in those who received the treatment compared to those who got a dummy drug.

It also can cause brain swelling and bleeding, side effects that can be dangerous in rare cases.

The drug received full approval last year from the U.S. Food and Drug Administration. Regulators in several other countries also have approved it.

The FDA also approved in July a competing drug from Eli Lilly and Co.

WASHINGTON — A unique peek inside the human brain may help explain how it clears away waste like the kind that can build up and lead to Alzheimer’s disease.

Brain cells use a lot of nutrients which means they make a lot of waste. Scientists have long thought the brain has special plumbing to flush out cellular trash, especially during sleep – they could see it happening in mice. But there was only circumstantial evidence of a similar system in people.

Now researchers have finally spotted that network of tiny waste-clearing channels in the brains of living people, thanks to a special kind of imaging.

“I was skeptical,” said Dr. Juan Piantino of Oregon Health & Science University, whose team reported the findings Monday. “We needed this piece to say this happens in humans, too.”

The study was published in the journal Proceedings of the National Academy of Sciences.

The brain is remarkably active during sleep. One reason seems to be that’s the time it does a deep clean. And that’s gotten attention because while losing a good night’s sleep muddles people’s thinking, chronic sleep deprivation also is considered a risk factor for dementia.

So how does the brain cleanse itself?

Over a decade ago, scientists at the University of Rochester first reported finding a network they dubbed the “glymphatic system.” Cerebrospinal fluid uses channels surrounding blood vessels to get deep into tissue and move waste until it exits the brain. When mice were injected with a chief Alzheimer’s culprit named beta-amyloid, it cleared away faster when the animals were sleeping.

It’s not clear exactly how that network works although some research has shown the pulsing of the blood vessels helps move the waste-clearing fluid where it needs go.

But it’s been hard to find that system in people. Regular MRI scans can spot some of those fluid-filled channels but don’t show their function, Piantino said.

So his team in Oregon injected a tracer into five patients who were undergoing brain surgery and needed a more advanced form of MRI. The tracer “lit up” under those scans and sure enough, 24 to 48 hours later, it wasn’t moving randomly through the brain but via those channels just like prior research had found in mice.

It’s a small but potentially important study that Rochester’s Dr. Maiken Nedergaard predicted will increase interest in how brain waste clearance connects to people’s health.

But to test if better sleep or other treatments might really spur waste clearance and improve health, “I have to be able to measure glymphatic function in people,” added Dr. Jeff Iliff of the University of Washington, who helped pioneer waste-clearance research. The question is whether the new study might point to ways of measuring.

Sleep isn’t the only question. For example, animal studies show an old blood pressure drug now used to treat PTSD may improve glymphatic function, and Iliff and colleague Dr. Elaine Peskind are about to study it in certain patients.

Additional larger studies in healthy people are needed and Piantino, whose lab focuses on sleep health, wants to find an easier, more noninvasive test.

“We cannot study all these questions by injecting people,” he said.

-___

The Associated Press Health and Science Department receives support from the Howard Hughes Medical Institute’s Science and Educational Media Group. The AP is solely responsible for all content.