An experimental treatment seems to delay the symptoms of Alzheimer’s evil in some genetically destined to suffer from the age of 40 and 50, according to new findings of an ongoing investigation, which is now delayed and entangled in bureaucratic obstacles for delays in the financing of the Government of Donald Trump.
The first results – a scientific scoop – were published on Wednesday, even when study participants feared that politics could limit their access to treatment that could save lives.
“It is still a study, but it has given me an extension of my life that I never imagined,” said Jake Heinrichs, one from New York City.
Now with 50 years, Heinrichs has been treated in that study for more than a decade and remains asymptomatic despite inheriting a gene causing Alzheimer’s that killed his father and his brother approximately at the same age.
If the financing lock stops the doses that Heinrich receives, “How long is we left?” Asked his wife, Rachel Chavkin. “This essay is life.”
Two medications marketed in the US can slightly delay the worsening of Alzheimer’s in its initial phases by eliminating from the brain one of its distinctive characteristics, a sticky substance called amyloid. However, until now, there were no indications that eliminating the amyloid before (many years before the appearance of the first symptoms) could postpone the disease.
The research, directed by the University of Washington in San Luis, involves families that transmit rare genetic mutations, which practically guarantees that they will develop symptoms at the same age as their affected relatives. This information helps scientists determine if treatments are taking effect.
The new findings focus on a subgroup of 22 participants who received drugs to eliminate amyloid for a longer time, an average of eight years. The prolonged elimination of amyloid reduced the risk of symptoms, researchers reported Wednesday in Lancet Neurology magazine.
Despite the small studio size, “it is incredibly important,” said David Gate, a neuroscientist from the Northwestern University, who did not participate in the investigation.
Now, participants have changed an experimental drug before Leqembi, an intravenous treatment approved in the US, to try to answer the following question.
“What we want to determine in the next five years is the effectiveness of protection,” said Dr. Randall Bateman, from the University of Washington, who directs the Alzheimer’s network of dominant inheritance, which includes studies in families with these rare genes. “Will the symptoms of Alzheimer’s disease ever present if we continue to treat them?”
The concern is as follows: Bateman raised funds to initiate that confirmatory study while looking for financing from the National Health Institutes (NIH) for the complete project, but its subsidy has been delayed due to the cancellation of mandatory revisions. This is an example of how millions of dollars in investigation have been paralyzed while NIH deal with financing restrictions and mass dismissals.
At the same time, the researchers wonder if NIH will divert their attention from Amiloid research after the comments of Dr. Jay Bhattacharya, nominated as the new director of the agency.
“One of the reasons why I think we have not advanced as much as we should in the treatment of Alzheimer’s is because NIH have not supported a sufficiently wide range of hypotheses,” Bhattacharya told Senators, responding to one who mentioned an example of previous scientific bad praxis, not related to current research.
Scientists do not know the exact cause of Alzheimer’s, a disease that destroys the mind and affects almost 7 million Americans, mainly in advanced stages of life. What is clear is that silent changes occur in the brain at least two decades before the first symptoms, and that sticky amyloid is an important factor. At some point, the accumulation of amyloid seems to trigger neuronal destruction by a protein called Tau, which causes cognitive deterioration.
Drugs are being tested that fight tau. Researchers also study other factors, such as inflammation, immune cells of the brain and certain viruses.
The NIH approach expanded as the researchers found more possible guilty. In 2013, the National Institute on Aging of NIH financed 14 clinical trials of possible drugs for Alzheimer’s, more than a third of which focused on amyloid. For the past fall, 68 clinical trials had been performed and approximately 18% focused on the amyloid.
Gate, from Northwestern, is counted among scientists who “believe that amyloid is not everything,” but said that nothing has invalidated the amyloid hypothesis. Recently, he used cerebral tissue preserved from an ancient amyloid study to understand how immune cells called Microglia can eliminate these plates and then contribute to brain regeneration, possible clues to improve modest current therapies.
For now, the amyloid is clearly involved in some way, and families with genes causing Alzheimer are helping to answer a crucial question for anyone at risk: Can the blockade of the accumulation of amyloid really prevent symptoms? Without the financing of the NIH, Bateman said, that opportunity will be lost.
“It’s absolute madness,” said June Ward, a study participant for a long time, who lives near Asheville, North Carolina, and plans to ask their friends to present complaints before legislators.
Ward turns 64 in June and is healthy, two years older than when his mother’s symptoms appeared. “It is exciting to think about the possibility that Alzheimer’s disease is not what kill me,” he said.
In New York, Heinrichs said he has the hope that his 3 -year -old son does not “suffer the stress and sadness that I lived as a young man when I saw my father fading.”
“We need NIH not to get politicized,” added Chavkin, his wife. “It’s simply to keep people alive or help them live better. And in this case, it’s helping my husband survive.”
